Where do gut bacteria come from in different organisms

We know that some of the bacteria in our gut come from the food we eat and our environment. I want to know if there is evidence of bacteria being transferred from the mother to her fetus or from the mother to the eggs.

I'm currently working with insects that have plastic-eating bacteria in their gut. They are raised in isolated spaces so those bacteria would have to come from the bran they eat or from their mother. I'm a physics student interested in biophysics so my biology knowledge is still a work in progress. Thank you.

For technical information on the subject, perhaps start with "vertical transmission insect symbionts" on google, which will lead to you to a variety of info's. Studies for symbionts of lice, fruit flies, mosquitos, termites, isopods, stinkbugs, butterflies and planthoppers.

Insect Symbiosis Vol 3 page 145 states:

Insects have been shown to use transovarian, egg smearing, and coprophagy, transmission, else entirely from the environment at every generation. There is a list of summaries of different insects that use different methods.

this also has masses of information:

Samples for large insects are taken with tweezers, small insects can be dunked in alcohol and then microbes are extracted. Microbia RNA can be checked for evidence if the symbionts come from the parents. You can probably figure out a variety of methods for transmitting your insects symbionts, simply applying the wanted gut bacteria to the substrate of new cultures. I expect it can work in between species. you can try smearing eggs too.

The composition of gut bacteria almost recovers after antibiotics

The trillions of bacteria in the human gut affect our health in multiple ways including effects on immune functions and metabolism. A rich and diverse gut microbiota is considered to promote health providing the human host with many competences to prevent chronic diseases. In contrast, poor diversity of the gut ecosystem is a characteristic feature of chronic diseases including obesity, diabetes, asthma and gut inflammatory disorders.

Due the general bacterial-killing nature of antibiotics, it has been speculated that repetitive use of antibiotics deprives people of a rich gut bacterial environment and through this lead to adverse health effects.

Now, an international team of researchers led from the University of Copenhagen and Steno Diabetes Center Copenhagen report when 3 antibiotics were given to young healthy men for 4 days it caused an almost complete eradication of gut bacteria, followed by a gradual recovery of most bacterial species over a period of six months.

After the six months, however, the study participants were still missing nine of their common beneficial bacteria and a few new potentially non-desirable bacteria had colonized the gut. The findings are published today in Nature Microbiology.

"We show that the gut bacterial community of healthy adults are resilient and able to recover after short-term simultaneous exposure to three different antibiotics However, our findings also suggest that exposure to broad-spectrum antibiotics may dilute the diversity of the intestinal bacterial ecosystem. Antibiotics can be a blessing for preserving human health but should only be used based upon clear evidence for a bacterial cause of infection," explains study lead , Professor Oluf Pedersen, Novo Nordisk Foundation Center for Basic Metabolic Research.

Is the missing beneficial gut microbes in the Western world due to over usage of antibiotics?

The study is a four-day intervention with three broad-spectrum so-called "last-resort" antibiotics in 12 adult healthy men. The method with a cocktail of three antibiotics was designed to mimic actual treatments in intensive care units.

The gut is a reservoir of hundreds of different bacterial species with antibiotic-resistant genes. This was confirmed in the study as these bacterial genes were the initiating force that led to the replenishment of bacteria in the gut.

"In this case, it is good that we can regenerate our gut microbiota which is important for our general health. The concern, however, relates to the potentially permanent loss of beneficial bacteria after multiple exposures to antibiotics during our lifetime. There is evidence that Western populations have a considerably lower diversity of their gut microbiota that native people living in certain parts of Africa and Amazonas. One possible explanation for this may be the widespread use of antibiotics in treatment of infectious diseases," says Oluf Pedersen.

I had the bacteria in my gut analysed. And this may be the future of medicine

W e are all familiar with "gut feelings", "gut reactions" and "gut instincts", but how much do we really know or care about our guts? As we become increasingly more aware of what we put in our stomachs, it's striking how ignorant we remain of what takes place in our intestines. And it turns out there is an awful lot going on down there.

Microbiologists have made some startling advances in revealing our innermost secrets. It turns out that there is a complex ecosystem deep within us that is home to a fantastic diversity of life – of which very little belongs to our species.

For most of us, suspicious of foreign bodies, it's a struggle to comprehend that at our very core we are less than – or rather much more than – human. But, the fact is, there are about 100 trillion organisms living in the gut. If you put them all together they would be about the size of a football. In terms of cells, the microbial kind outnumber their human counterparts by about three to one. And in terms of genes, the microbial advantage is more like 300 to one.

That means there is a tremendous amount of us that is not, so to speak, us. This raises a whole range of interesting philosophical and anatomical questions, of which the most urgent might be: should we be worried?

Well, I wasn't much concerned about bacteria before I got the contents of my gut tested. I took a fairly relaxed view that as long as the lavatory was regularly bleached, I brushed my teeth and kept the kitchen surfaces reasonably clean then I didn't have to think too much about what goes on at the microbial level. But there's nothing like spooning your own faecal matter into a Perspex container to make you stop and contemplate just what it is that we're full of. That unpleasant task is precisely what I found myself doing last October, as I gathered a stool sample to send off, cold-packed to the BioSciences Institute at University College Cork in Ireland.

The institute is one of Europe's leading centres for the study of what is now referred to as the microbiome – that is all the bacteria, viruses, fungi, archaea and eukaryotes that inhabit the human body, inside and out. The simplistic view of these guests has traditionally centred on their parasitic or pathogenic aspects. Either they were fairly harmlessly hitching a free ride or were a direct threat to their host.

But the latest thinking presents this vast army of microbes as a vital component in furnishing and maintaining human health. Such is the microbiome's importance that it is now viewed by scientists as a separate organ with its own dynamic metabolic activity. But what precisely is that activity and is it all going to plan with me?

Paul O'Toole is a professor at the Alimentary Pharmabiotic Centre, which is part of the BioSciences Institute at Cork. A keen marathon runner, he looks like he knows a thing or two about intestinal fortitude. He co-ordinated a government-funded study – fortuitously launched just before the Irish economy collapsed – entitled Eldermet, which was aimed at helping the Irish food industry develop food products for old people. To do that, they needed a knowledge base of the gut microbiota. So O'Toole began examining how diet affects the microbiota of Ireland's elderly population.

There is an element of poacher-turned-gamekeeper to his career because he started out as something of a bacterial enemy. "I spent about 15 years working on pathogens where you're trying to kill them," he tells me in his office. "I did my PhD in staphylococcus. One organism, one gene. I worked on a condition called scalded skin syndrome syndrome where staphylococci infect the umbilical stump and if they produce a toxin all the baby's skin peels off."

From combatting staphylococci, he moved into probiotics – the organisms that are supposed to be good for us – which in commercial form have been decanted into capsules and yoghurts and advertised to the public as "friendly bacteria". But he discovered that he couldn't effectively study probiotics in isolation because their benefits were often indirect.

"I realised I needed to study the whole canvas," he says. And that was how he came to find himself involved with the microbiome, just when it was starting to become the subject of intensive biomedical research.

There are two labs, O'Toole explains, that processed my sample. The first was the wet lab, where, through various molecular assaults, DNA was extracted, 95% of which was bacterial. This was then sent to an external company to be sequenced – there were over 30,000 sequences – and then a huge file of data was crunched by what O'Toole called "a bunch of computer nerds who sit around all day generating stats" in the institute's data lab.

Just a year ago, that process cost upwards of £400. Now it can done for as little as £15. What you get are a couple of pie charts that list the microbiota found in the gut at different phylogenetic levels and a narrative explanation as to what their significance is. Phylogentic levels in this instance simply refer to different levels of resolution.

At the broadest level, the phylum level, my microbiota, in common with everyone else's, was dominated by two types: firmicutes and bacteroidetes. The western diet, by which we tend to mean the North American diet, is high in fat and protein. In this diet bacteroidetes usually make up more than 55% of the gut microbiota, and sometimes, in North America itself, as much as 80%. In Europe, the average numbers vary from country to country. In my case I had 34%.

The opposite to a North American diet is what O'Toole calls a "natural diet". "Our antecedents on the plains of Africa weren't chewing on burgers," he explains. "They were running around eating plant foods and leaves and occasionally eating a squirrel if they were lucky."

On a plant-based diet, the microbiota is tipped in favour of the other major phylum, firmicutes. Some of the complex carbohydrates in plants cannot be digested by our bodies alone. They have to be broken down by the gut microbiota, which produce enzymes to chop up the long chains and ferment them into short-chain fatty acids such as butyrate – which is made exclusively by bacteria – acetate and propionate.

These fatty acids are beneficial to the body. Butyrate, for example, provides an energy source that the cells lining our intestines can directly access. It also controls the proliferation of cells in the intestine and is thought to possess anti-carcinogenic properties. All of which meant that my score of 51% firmicutes was a healthy sign.

Zooming into the genus level, which offers a more detailed look at my microbial composition, the good news continued. I had three times as much of the butyrate-producing roseburia than the healthy cohort used in O'Toole's study. Many more lachnospira than normal but many fewer bacteroides (not to be confused with bacteroidetes) and alistipes – as O'Toole put it, in more scientific terms, "bugger all".

Again these were positive results. Lachnospira degrade pectins and ferment dietary fibres and I have three times more than typical. And bacteroides are often associated with meat-based, high-protein, high-fat diets, just as alistipes tend to be more present in people who eat less plant-based food. In sum that meant my gut – the lack of six-pack notwithstanding – was probably in good shape. Of course, it's not the sort of thing you can boast about at dinner parties. "I've got significantly higher than average amounts of lachnospira," is unlikely to be a conversational gambit that will impress non-microbiologists, even if you do manage to pronounce the word correctly. But just as we now know that high cholesterol is something to be avoided, so too might we soon begin to become aware of the sorts of bacteria counts that are markers for good health, especially as the price of testing comes down.

There were, however, one or two results that O'Toole struggled to make sense of. In particular my high levels of natranaerobius, a genus of bacteria that thrive in high-salt, highly alkaline environments. Did I eat a lot of sushi? No, while I love fish, I tend to prefer it cooked. Did I prepare a lot of fish? No more than once a week.

Although he found nothing sinister in the natranaerobius, it perturbed him that he couldn't quite put his finger on the cause of its abundance in my gut. But by then he had managed to make a blind prediction of my diet that was uncannily accurate. He saw very little evidence of meat-eating – I haven't eaten meat for 30 years. But there was plenty of evidence of high fibre, which is good because bacteria feed on fibre. If we don't feed bacteria, they feed off us – specifically the mucus lining in our large intestine. There was also evidence of lots of fish and a large range of vegetables. All of which exactly represents my diet.

I suggest that it must be satisfying to get his prediction so right.

"It's a bit spooky all right," he agrees. "But it made me think about the utility of it. I mean, it's not particularly useful to tell people what they eat."

O'Toole is interested in the diagnostic potential of the microbiome. "We could probably guess what your inflammatory parameters are," he says, fixing me with one of those expressions in which GP's specialise when looking up from studying your medical notes: neutral, unyielding, and anxiety-inducing. Not only do I not know what my inflammatory parameters are, I don't know what inflammatory parameters means.

O'Toole explains that significant links have been established between gut microbiota and inflammation, sarcopenia and cognitive function.

"Inflammation," he says, "is not a swollen thumb. Inflammation means how activated your immune system is. I would guess that your inflammatory markers are baseline. Flat. In old people they're not. In old people, the immune system is typically turned on and that's not good, because if it's turned on, when they get a winter flu all their energies are expended chasing ghosts. So you want to turn down the inflammation."

Sarcopenia means loss of muscle mass. It happens as we get older because the body becomes less efficient at turning protein into muscle, which is why older people need to have more protein. "We think that the narrowing of gut bacteria in old people is making the intestine less efficient at absorbing proteins," says O'Toole.

Cognitive function is partly related to what's known as the brain-gut axis. As all those phrases like "gut wrenching" and "gut feeling" suggest, there is indeed an intimate link between the brain and the gut. Our intestines are acutely responsive to shifts in our emotions and mental states. But it's a two-way street: studies suggest that our brains and emotions are also sensitive to what's going on in our guts.

T ypically, cognitive function is only slowly diminished as we get older, but in some cases it can quickly accelerate.

"There are physiological reasons like Alzheimer's and senile dementia that explain rapid cognitive impairment," O'Toole says. "But the rate of loss could also be affected by compounds made by bacteria, and that's what we're targeting. Bacteria produce chemicals which are analogues – in other words they look identical to normal human transmitters. What we hope is that we can improve the ability of old people to process data."

Common to all these issues, particularly among the aged, is the narrowing of the gut microbiota which, in turn, is usually the result of a narrowing of diet. This is a point that O'Toole repeatedly emphasises.

"Diversity is the key. What we see with people on narrow diversity diets is that the microbiota collapses. A good analogy would be an ecosystem like a rainforest, where you've got loads of plants and animals interacting. It's evolved over tens of thousands of years, then one of the key species, a tree, gets cut down and you get ecological collapse.

"And if you had a gentleman whose wife died and she had done all the cooking, and then he's suddenly eating toast and marmalade, the diversity of gut microbiota will collapse – because diversity of diet correlates with diversity of microbiota – and you will get a range of health problems associated with that."

He goes on to tell me that my microbial diversity is impressively wide and that, by way of summary, he would suggest that my diet is "pretty bloody good". Forget the 5-2 diet, I suddenly feel like writing a bestselling diet book entitled Guts: The Microbial Guide to Healthy Eating. In one sense, of course, it's no great achievement. Studies show that it only takes a short time of a changed diet to dramatically change the microbiota, although it changes back just as quickly as soon as the diet is dropped.

But this apparently superficial relationship between food and microbes is in reality rather profound because first it speaks of a co-evolution with the human body over tens of thousands of years. Like all organisms and species, humans have evolved to have a particular relationship with a particular set of microbes.

There are hundreds of thousands of kinds of microbes on Earth but only about a thousand enjoy an association with humans. Thus, secondly it suggests that we need to stop thinking of ourselves as separate entities from the microbes that have colonised our bodies.

"We came through the period of medicine in which we developed antibiotics," says O'Toole. "Until the second world war we were dying from stupid things like pneumonia and galloping septicemia from a small wound. So antibiotics were a major success. Then we've had the backlash where we've prescribed them too much and can't control the pathogens. But now we have a more intelligent understanding of humans as chimeras."

A germ-free existence would be an unhappy one. Tests have shown that a mouse raised in a lab devoid of bacteria fails to develop a proper immune system or an effective digestive system. It has to consume a lot more food to extract calories. Humans are first colonised by microbes during birth. Then through breast milk, which contains both probiotics (beneficial microbes) and prebiotics (compounds that foster the growth of probiotics).

"There is strengthening evidence," says O'Toole, "that the explosion of auto-immune diseases and immune disregulation diseases in western society may be due to suppression of gut bacteria from infancy onwards.

"The immune system in babies is probably taught to distinguish between self and non-self in the context of bacteria. There are two recent papers in the publication Nature showing that butyrate is important in enlisting regulatory T-cells, a branch of immune cells that control the processes involved in inflammatory bowel disease and irritable bowel syndrome."

It takes about two years from birth through a process of selection for a child to attain a mature microbiome. There are several phenomena that may contribute to childhood microbial diminishment. One is the increase in caesarian sections.

"Babies who were previously colonised in the birth canal with their mother's microbiota now have a gut microbiota that is more like the walls of the hospital than it is mum's vaginal microbiota."

Another is lack of breast milk, and a third is the increased use of antibiotics. O'Toole says that one study suggests that repeated use of antibiotics tips the microbiota towards one that promotes obesity. In fact there are many studies around the globe that are still in their infancy but which point up connections between the microbiota and diseases and complaints as diverse as irritable bowel syndrome, inflammatory bowel disease, type-two diabetes, Parkinson's, Alzheimer's, autism, depression, cardiovascular disease and colon cancer.

But so far none of it is conclusive and much is highly speculative. After the initial claims about the potential health benefits of microbiome research – the kind that tend to help funding – there has been a bit of a sceptical backlash.

Several articles have pointed out that there has been plenty of hyperbole but not enough substance. And as yet the medical profession isn't rushing to produce microbiome specialists.

"Medicine is notoriously slow to adopt new ideas," says O'Toole. He cites the case of Barry Marshall, an Australian doctor whose claim to have established a bacterial cause of peptic ulcers and gastric cancer was comprehensively ridiculed by the medical establishment in the 1980s. "About 20 years later he got the Nobel prize."

The problem, he says, is that microbiologists have been very good at discovering gut bacteria and identifying what roles they might play, but they have been slow to develop mechanisms to establish firm causal links and practical applications.

"I personally hope it doesn't become the solution for everything because it's not going to be credible, it's simply not true. There's plenty of evidence that most human major diseases have a physiological or lifestyle basis, but it's probable in some of those that the gut microbiota is a modulating factor that contributes to the overall risk."

Right now, O'Toole would like to like to reduce the lower diversity microbiota in the elderly by means of dietary supplements. "But we worry that, as the World Wildlife Fund says, extinction may be forever. That if a particularly good bacterium is missing from an elderly person, we may not be able to get it back by diet alone."

The solution in that case might be fecal microbiota transplantation, which O'Toole helpfully clarifies, "is the idea of transplanting someone else's poo into a recipient". Which neatly brings us back to where I started. If collecting your own excrement is counter-intuitive, then injecting it into someone else runs against every decent human instinct.

But it's already happening in North America and O'Toole suggests that such transplants may help prevent ulceration of the colon – a condition that nearly killed my father some years back.In the end, it's all comes back to what you put in and take out. And in that tireless cycle of life, we shouldn't be appalled if not even our waste need go to waste.

Please note: the BioSciences Institute is not able to offer individual analysis, and did so for the purposes of this piece only.

How Gut Bacteria Tell Their Hosts What to Eat

Scientists have known for decades that what we eat can change the balance of microbes in our digestive tracts. Choosing between a BLT sandwich or a yogurt parfait for lunch can increase the populations of some types of bacteria and diminish others&mdashand as their relative numbers change, they secrete different substances, activate different genes and absorb different nutrients.

And those food choices are probably a two-way street. Gut microbes have also been shown to influence diet and behavior as well as anxiety, depression, hypertension and a variety of other conditions. But exactly how these trillions of tiny guests&mdashcollectively called the microbiome&mdashinfluence our decisions on which foods to stuff into our mouths has been a mystery.

Now neuroscientists have found that specific types of gut flora help a host animal detect which nutrients are missing in food and then finely titrate how much of those nutrients the host really needs to eat. &ldquoWhat the bacteria do for appetite is kind of like optimizing how long a car can run without needing to add more petrol to the tank,&rdquo says senior author Carlos Ribeiro, who studies the eating behaviors of Drosophila melanogaster, a type of fruit fly, at Champalimaud Center for the Unknown in Lisbon.

In a paper published recently in PLOS Biology, Ribeiro and his team demonstrated how the microbiome influences drosophila&rsquos nutritional decisions. First, they fed one group of flies a sucrose solution containing all the necessary amino acids. Another group got a mix that had some of the amino acids needed to make protein but lacked essential amino acids that the host cannot synthesize by itself. For a third group of flies, the scientists removed essential amino acids from the food one by one to determine which was being detected by the microbiome.

After 72 hours on the various diets, flies in the all three groups were presented with a buffet offering their usual sugary solution alongside protein-rich yeast. The researchers found that flies in the two groups whose diet lacked any single essential amino acid got a strong craving for yeast to make up for the missing nutrients. But when scientists increased five different types of bacteria found in the flies&rsquo digestive tracts&mdashLactobacillus plantarum, L. brevis, Acetobacter pomorum, Commensalibacter intestini and Enterococcus faecalis&mdashthe flies completely lost the urge to eat more protein.

The researchers found that the flies&rsquo amino acid levels were still low, indicating the bacteria were not simply replacing nutrients missing from the flies&rsquo diet by producing the amino acids themselves. Instead the microbes were functioning as little metabolic factories, transforming the food they got into new chemicals: metabolites that the researchers believe might be telling the host animal it could carry on without the amino acids. As a result of this microbial trick, the flies were able to continue reproducing, for example&mdasheven though an amino acid deficiency usually hampers cell growth and regeneration and therefore reproduction, Ribeiro explains.

Two kinds of bacteria were particularly effective in influencing the appetites of flies this way: Acetobacter and Lactobacillus. Increasing both was enough to suppress the flies&rsquo protein cravings and increase their appetite for sugar. These two bacteria also restored the flies&rsquo reproductive abilities, indicating their bodies were carrying out normal functions that typically get restricted when there is a nutritional deficiency. &ldquoHow the brain handles this trade-off of nutritional information is very fascinating, and our study shows that the microbiome plays a key role in telling the animal what to do,&rdquo Ribeiro says.

Next the team removed an enzyme needed to process the amino acid tyrosine in flies, making it necessary for the flies to get tyrosine via their food, just like other essential amino acids. Surprisingly, they found that Acetobacter and Lactobacillus were unable to suppress the craving for tyrosine in the modified flies. &ldquoThis shows that the gut microbiome has evolved to titrate only the normal essential amino acid intake,&rdquo Ribeiro explains.

The research adds a new perspective on coevolution of microbes and their hosts. &ldquoThe findings show there is a unique pathway that has coevolved between animals and the resident bacteria in their gut, and there is a bottom-up communication about diet,&rdquo says Jane Foster, who is a neuroscientist at McMaster University in Ontario and not associated with the study.

Although the research does not specify the exact mechanism of communication, Ribeiro thinks it could take different forms. Strong evidence from the study indicates that microbially derived metabolites carry information from the gut to the brain, telling the host whether it needs a particular kind of food. &ldquoOne of the big evolutionary mysteries is why we lost the ability to produce essential amino acids,&rdquo he says. &ldquoMaybe these metabolites gave animals more leeway to be independent of these nutrients and to deal without them sometimes.&rdquo

Microbes may have their own evolutionary reasons for communicating with the brain, he adds. For one thing, they feed on whatever the host animal eats. For another, they need host animals to be social so the guests can spread through the population. The data are limited to animal models so far, but Ribeiro believes that gut-brain communication can provide fertile ground for developing treatments for humans in the future. &ldquoIt&rsquos an interesting therapeutic window that could be utilized to improve behaviors related to diet one day,&rdquo he says.

How can I increase good bacteria in my gut?

1. Fill Up on Fiber.

High-fiber foods feed the healthy bacteria that improve immune function, reduce inflammation and chronic disease, and even help regulate mood.

2. Pick Prebiotic-Rich Foods.

Prebiotics feed healthy bacteria. Good sources of prebiotics include Jerusalem artichokes, chicory root, raw dandelion greens, leeks, onions, garlic, asparagus, whole wheat, spinach, beans, bananas, oats, and soybeans.

3. Try Probiotic Foods.

Probiotics are live bacteria or yeasts found in fermented foods that, when consumed, take up residence in the gut and improve health. Healthy sources include sauerkraut, miso, tempeh, kimchi, and water kefir.

4. Avoid Animal Products.

Red meat, high-fat dairy products, and fried foods all reduce the growth of healthy bacteria and enhance the growth of “bad” bacteria linked to chronic disease.

5. Limit Fats.

Avoid fried foods, saute with cooking spray or broth instead of oil, and use low-fat salad dressings, especially if you have diabetes or prediabetes. Most plant foods are naturally low in fat.

6. Avoid Unnecessary Antibiotics.

Overuse of antibiotics can kill off healthy bacteria. The U.S. Food and Drug Administration estimates that 80 percent of antibiotics are actually used in animal agriculture.

7. Practice a Healthy Lifestyle.

Exercising, getting enough sleep, and managing stress can all have a positive impact on your gut microbes.


We are a product of our environment.

As infants we (and our guts) come into this world with a blank slate of sorts, awaiting our first contact with the microscopic organisms which surround us. Our first exposure via the birth canal, followed by a gut-nurturing concoction of mother’s milk, is nature’s way of establishing the foundation on which we will build our microbiome. Familial, dietary, and environmental exposure throughout our developing years cultivates an ecosystem which will play a starring role in the determination of our health for a lifetime.

In fact, every time you kiss someone, every time you pet an animal, each time you eat a meal or apply a cosmetic, you are affecting the composition of your microbiome.

What’s Up With the Bacteria in Your Gut?

The overuse of antibiotics, eating processed foods, and a generally sanitized lifestyle in industrialized nations is contributing to people's ill health and many modern plagues.

Biology, Health, Social Studies

Beneficial Gut Bacteria

Gut bacteria, which form our microbiome, play an essential role in our emotional health as well as our physical health. Fiber-rich prebiotic foods, like fruits, vegetables, and whole grains as well as probiotic fermented foods such as yogurt, sauerkraut, kimchi, and miso soups are recommended for our microbiome.

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Your gut is home to a rich collection of bacteria that play an important part in digestion. Our guts, or intestines, produce enzymes, which are substances that help break down food. Sometimes, our enzymes can't deal with certain foods, like beans. That's when our gut bacteria step in. They chomp down on those bean molecules, creating gas in the process.

But gut bacteria do much more than play a role in human nutrition. The key to whether we're fat or thin, cheerful or depressed, healthy or sick may lie in the gut microbiome. A microbiome is the collection of microorganisms, like bacteria, in a particular place. Your gut's microbiome is home to hundreds of species of bacteria.

Poop Is Everywhere, But That's A Good Thing

You start collecting your gut bacteria at birth, when you pass through your mother's birth canal. You pick up even more bacteria through your mother's milk. Milk contains substances that can only be digested by bacteria, specifically by Bifidobacterium infantis. This is a helpful bacterium that makes itself at home in the baby's digestive passage and helps prevent infections. Milk also functions as a probiotic, or a substance that helps good bacteria grow. In addition, milk is a prebiotic. This means that it supplies your gut bacteria with something to eat.

By the time kids turn 3, they are usually introduced to solid foods and can crawl around on the floor. By this age, their internal microbiomes are fully established. This means that they have come in contact with large numbers of fecal particles &mdash bits of poop. According to scientists who study microorganisms, the environment is pretty much coated in fecal particles.

It might sound creepy, but it is a good thing. The bacteria that we pick up can provide us with enzymes and vitamins. They help us battle infections, and they make chemicals necessary for our mental health and well-being. For example, serotonin is a chemical that sends signals between nerve cells, and it affects our mood, appetite, sleep, memory and learning. Ninety percent of the body's serotonin is made by gut bacteria.

Junk Food Can Kill Off Good Bacteria

Our personal bacteria also protect us from a wide range of illnesses. Scientists think that the increase in some sicknesses in the population means that something is going seriously wrong in terms of bacteria. The modern rise in the number of people who are overweight, have allergies, asthma, arthritis and anxiety attacks may be related to the bacterial populations in our guts.

The problem here might be a leaky epithelium. The epithelium is the lining of the digestive tract, and it usually acts as a barrier between your gut bacteria and the rest of the body. Bacteria keep epithelial cells healthy by providing them with nutrition. But without the right nurturing bacteria, the epithelium breaks down. Bacteria and toxic bacterial by-products enter the bloodstream. This sends a signal to the immune system, alerting it to the presence of invaders. This can lead to inflammation and, eventually, disease.

In industrialized nations like the United States, a sanitized lifestyle and a diet of processed foods have killed off some of our body's microorganisms. So have antibiotics, which are medicines that fight against bacterial infection. The result is a microbiome that does not have many helpful types of bacteria. Many modern diseases may be occurring because our microbiomes aren't what they used to be.

A diet of junk food doesn't do our bacteria any good, either. Tim Spector is a scientist who studies diseases. In an experiment, he convinced his adult son to spend 10 days on a dedicated fast-food diet of fries, burgers, chicken nuggets and Coca-Cola. By the end of 10 days, he had lost one-third of the bacterial species in his gut.

Exercising, Eating Fiber-Rich Foods Can Help

How can you keep your microbiome healthy? Scientists and doctors say that you should not depend too much on the probiotic supplements available in the market. Instead, they recommend a diet rich in probiotic fermented foods, or foods in which the molecules are broken down by yeast or bacteria. Examples include yogurt, sauerkraut, kimchi and miso soup. They also suggest fiber-rich foods, like whole grains, fruits and vegetables. It is also a good idea to avoid processed foods, which do not provide much nourishment for your gut bacteria.

Exercise also seems to benefit our guts. In one study, researchers compared rugby players to nonathletes and found that the rugby players had more diverse microbiomes, with higher proportions of at least 40 different bacterial species.

While antibiotics are sometimes necessary, we should be cautious about overusing them. Studies show that that the gut microbiome can take up to a year to bounce back after a course of antibiotics, which can wipe out lots of bacteria, both good and bad.

Finally, you might want to expand your environment. The more different kinds of bacteria you pick up, the better. So meet new people, pat the dog, dig in the garden and play in the dirt.

Microbes and Ecosystem Niches

Microbial life is amazingly diverse and microorganisms quite literally cover the planet. In fact, it has been estimated that there are 100,000,000 times more microbial cells on the planet than there are stars in the observable universe! Microbes live in all parts of the biosphere where there is liquid water, including soil, hot springs, the ocean floor, acid lakes, deserts, geysers, rocks, and even the mammalian gut.

By virtue of their omnipresence, microbes impact the entire biosphere indeed, microbial metabolic processes (including nitrogen fixation, methane metabolism, and sulfur metabolism) collectively control global biogeochemical cycling. The ability of microbes to contribute substantially to the function of every ecosystem is a reflection their tremendous biological diversity.

Figure: A Biofilm of Thermophilic Bacteria: Thermophiles, which thrive at relatively high temperatures, occupy a unique ecological niche. This image shows a colony of thermophilic bacteria at Mickey Hot Springs in Oregon, USA.

Microbes are vital to every ecosystem on Earth and are particularly important in zones where light cannot approach (that is, where photosynthesis cannot be the basic means to collect energy). Microorganisms participate in a host of fundamental ecological processes including production, decomposition, and fixation. They can also have additional indirect effects on the ecosystem through symbiotic relationships with other organisms. In addition, microbial processes can be co-opted for biodegradation or bioremediation of domestic, agricultural, and industrial wastes, making the study of microbial ecology particularly important for biotechnological and environmental applications.

Each species in an ecosystem is thought to occupy a separate, unique niche. The ecological niche of a microorganism describes how it responds to the distribution of resources and competing species, as well as the ways in which it alters those same factors in turn. In essence, the niche is a complex description of the ways in which a microbial species uses its environment.

The precise ecological niche of a microbe is primarily determined by the specific metabolic properties of that organism. For example, microbial organisms that can obtain energy from the oxidation of inorganic compounds (such as iron-reducing bacteria ) will likely occupy a different niche from those that obtain energy from light (such as cyanobacteria). Even among photosynthetic bacteria, there are various species that contain different photosynthetic pigments (such as chlorophylls and carotenoids) that allow them to take advantage of different portions of the electromagnetic spectrum therefore, even microbes with similar metabolic properties may inhabit unique niches.

What Happens Inside the Gut?

In many experiments, scientists use mice to represent humans. Like our microbiome, mice can also have about a billion bacteria in their guts. The scientists wanted to imitate the guts of people with colitis (the deadly disease caused by C. diff), so they gave the mice two treatments of antibiotics. For 12 days, the first antibiotic wiped out most of the mice’s microbes. Then the scientists fed the mice C. diff spores (with resistant covers).

For the next 21 days, the mice received no more antibiotics. This allowed C. diff and other microbes to grow back. Then the scientists treated the mice with another antibiotic for 7 more days. This antibiotic killed C. diff and the healthy good bacteria. After this treatment, C. diff were in a race with the heathy bacteria to see who could grow the quickest. C. diff won the race and caused disease.

After the treatments, scientists noted some changes in the mouse microbiome. Bacteria belonging to the G+ group (with a thicker coat) were more abundant than bacteria in the G- group. This meant that C. diff changed the mouse microbiome. Most likely, it was because C. diff produced para-cresol, as G- bacteria are more sensitive to para-cresol than G+ bacteria.

The Normal Gut Microbiota: An Essential Factor in Health

Basic Definitions and Development of the Microbiota

The term microbiota is to be preferred to the older term flora, as the latter fails to account for the many nonbacte-rial elements (eg, archea, viruses, and fungi) that are now known to be normal inhabitants of the gut. Given the relatively greater understanding that currently exists of the role of bacteria, in comparison with the other constituents of the microbiota in health and disease, gut bacteria will be the primary focus of this review. Within the human gastrointestinal microbiota exists a complex ecosystem of approximately 300 to 500 bacterial species, comprising nearly 2 million genes (the microbiome). 1 Indeed, the number of bacteria within the gut is approximately 10 times that of all of the cells in the human body, and the collective bacterial genome is vastly greater than the human genome.

At birth, the entire intestinal tract is sterile the infant’s gut is first colonized by maternal and environmental bacteria during birth and continues to be populated through feeding and other contacts. 2 Factors known to influence colonization include gestational age, mode of delivery (vaginal birth vs assisted delivery), diet (breast milk vs formula), level of sanitation, and exposure to antibiotics. 3 , 4 The intestinal microbiota of newborns is characterized by low diversity and a relative dominance of the phyla Proteobacteria and Actinobacteria thereafter, the microbiota becomes more diverse with the emergence of the dominance of Firmicutes and Bacteroidetes, which characterizes the adult microbiota. 5 – 7 By the end of the first year of life, the microbial profile is distinct for each infant by the age of 2.5 years, the microbiota fully resembles the microbiota of an adult in terms of composition. 8 , 9 This period of maturation of the microbiota may be critical there is accumulating evidence from a number of sources that disruption of the microbiota in early infancy may be a critical determinant of disease expression in later life. It follows that interventions directed at the microbiota later in life may, quite literally, be too late and potentially doomed to failure.

Following infancy, the composition of the intestinal microflora remains relatively constant until later life. Although it has been claimed that the composition of each individual’s flora is so distinctive that it could be used as an alternative to fingerprinting, more recently, 3 differ-ent enterotypes have been described in the adult human microbiome. 10 These distinct enterotypes are dominated by Prevotella, Ruminococcus, and Bacteroides, respectively, and their appearance seems to be independent of sex, age, nationality, and body mass index. The microbiota is thought to remain stable until old age when changes are seen, possibly related to alterations in digestive physiology and diet. 11 – 13 Indeed, Claesson and colleagues were able to identify clear correlations in elderly individuals, not only between the composition of the gut microbiota and diet, but also in relation to health status. 14

Regulation of the Microbiota

Because of the normal motility of the intestine (peristalsis and the migrating motor complex) and the antimicrobial effects of gastric acid, bile, and pancreatic and intestinal secretions, the stomach and proximal small intestine, although certainly not sterile, contain relatively small numbers of bacteria in healthy subjects. 15 Interestingly, commensal organisms with probiotic properties have recently been isolated from the human stomach. 16 The microbiology of the terminal ileum represents a transition zone between the jejunum, containing predominantly aerobic species, and the dense population of anaerobes found in the colon. Bacterial colony counts may be as high as 10 9 colony-forming units (CFU)/mL in the terminal ileum immediately proximal to the ileocecal valve, with a predominance of gram-negative organisms and anaerobes. On crossing into the colon, the bacterial concentration and variety of the enteric flora change dramatically. Concentrations of 10 12 CFU/mL or greater may be found and are comprised mainly of anaerobes such as Bacteroides, Porphyromonas, Bifidobacterium, Lactobacillus, and Clos-tridium, with anaerobic bacteria outnumbering aerobic bacteria by a factor of 100 to 1000:1. The predominance of anaerobes in the colon reflects the fact that oxygen concentrations in the colon are very low the flora has simply adapted to survive in this hostile environment.

At any given level of the gut, the composition of the flora also demonstrates variation along its diameter, with certain bacteria tending to be adherent to the mucosal surface, while others predominate in the lumen. It stands to reason that bacterial species residing at the mucosal surface or within the mucus layer are those most likely to participate in interactions with the host immune system, whereas those that populate the lumen may be more relevant to metabolic interactions with food or the products of digestion. It is now evident that different bacterial populations may inhabit these distinct domains. Their relative contributions to health and disease have been explored to a limited extent, though, because of the relative inaccessibility of the juxtamucosal populations in the colon and, especially, in the small intestine. However, most studies of the human gut microbiota have been based on analyses of fecal samples, therefore representing a major limitation. Indeed, a number of studies have already shown differ-ences between luminal (fecal) and juxtamucosal populations in disorders such as inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). 17 , 18

In humans, the composition of the flora is influenced not only by age but also by diet and socioeconomic conditions. In a recent study of elderly individuals, the interaction of diet and age was demonstrated, firstly, by a close relationship between diet and microbiota composition in the subjects and, secondly, by interactions between diet, the microbiota, and health status. 14 It must also be remembered that nondigestible or undigested components of the diet may contribute substantially to bacterial metabolism for example, much of the increase in stool volume resulting from the ingestion of dietary fiber is based on an augmentation of bacterial mass. The subtleties of interaction between other components of diet and the microbiota are now being explored and will, undoubtedly, yield important information. For example, data indicating a potential role of certain products of bacterial metabolism in colon carcinogenesis have already provided strong hints of the relevance of diet-microbiota interactions to disease. Antibiotics, whether prescribed or in the food chain as a result of their administration to animals, have the potential to profoundly impact the microbiota. 19 In the past, it was thought that these effects were relatively transient, with complete recovery of the microbiota occurring very soon after the course of antibiotic therapy was complete. However, while recent studies have confirmed that recovery is fairly rapid for many species, some species and strains show more sustained effects. 20

Host-Microbiota Interactions

Gut-commensal microbiota interactions play a fundamental role in promoting homeostatic functions such as immunomodulation, upregulation of cytoprotec-tive genes, prevention and regulation of apoptosis, and maintenance of barrier function. 21 The critical role of the microbiota on the development of gut function is amply demonstrated by the fate of the germ-free animal. 22 , 23 Not only are virtually all components of the gut-associated and systemic immune systems affected in these animals, but the development of the epithelium, vasculature, neu-romuscular apparatus, and gut endocrine system also is impaired. The subtleties of the interactions between the microbiota and the host are exemplified by studies that demonstrate the ability of a polysaccharide elaborated by the bacterium Bacteroides fragilis to correct T-cell deficien-cies and Th1/Th2 imbalances and direct the development of lymphoid organs in the germ-free animal. 24 Intestinal dendritic cells appear to play a central role in these critical immunologic interactions. 24 , 25

How does the gut immune system differentiate between friend and foe when it comes to the bacteria it encounters? 26 At the epithelial level, for example, a number of factors may allow the epithelium to tolerate commensal (and thus probiotic) organisms. These include the masking or modification of microbial-associated molecular patterns that are usually recognized by pattern recognition receptors, such as Toll-like receptors, 27 and the inhibition of the NF㮫 inflammatory pathway. 28 Responses to commensals and pathogens also may be distinctly different within the mucosal and systemic immune systems. For example, commensals such as Bifidobacterium infantis and Faecalibacterium prausnitzii have been shown to differentially induce regulatory T cells and result in the production of the anti-inflammatory cytokine interleukin (IL)-10. 29 Other commensals may promote the development of T-helper cells, including TH17 cells, and result in a controlled inflammatory response that is protective against pathogens in part, at least, through the production of IL-17. 30 The induction of a low-grade inflammatory response (physiologic inflammation) by commensals could be seen to prime the host’s immune system to deal more aggressively with the arrival of a pathogen. 31

Through these and other mechanisms, the microbiota can be seen to play a critical role in protecting the host from colonization by pathogenic species. 32 Some intestinal bacteria produce a variety of substances, ranging from relatively nonspecifc fatty acids and peroxides to highly specific bacteriocins, 33 , 34 which can inhibit or kill other potentially pathogenic bacteria, 35 while certain strains produce proteases capable of denaturing bacterial toxins. 36

The Microbiota and Metabolism

Although the immunologic interactions between the microbiota and the host have been studied in great detail for some time, it has been only recently that the true extent of the metabolic potential of the microbiota has begun to be grasped. Some of these metabolic functions were well known, such as the ability of bacterial disac-charidases to salvage unabsorbed dietary sugars, such as lactose, and alcohols and convert them into short-chain fatty acids (SCFAs) that are then used as an energy source by the colonic mucosa. SCFAs promote the growth of intestinal epithelial cells and control their proliferation and differentiation. It has also been known for some time that enteric bacteria can produce nutrients and vitamins, such as folate and vitamin K, deconjugate bile salts, 37 and metabolize some medications (such as sul-fasalazine) within the intestinal lumen, thereby releasing their active moieties. However, it is only recently that the full metabolic potential of the microbiome has come to be recognized and the potential contributions of the microbiota to the metabolic status of the host in health and in relation to obesity and related disorders have been appreciated. The application of genomics, metabolomics, and transcriptomics can now reveal, in immense detail, the metabolic potential of a given organism. 38 – 41

It is now also known that certain commensal organisms also produce other chemicals, including neurotrans-mitters and neuromodulators, which can modify other gut functions, such as motility or sensation. 42 – 44 Most recently and perhaps most surprisingly, it has been proposed that the microbiota can influence the development 45 and func-tion 46 of the central nervous system, thereby leading to the concept of the microbiota-gut-brain axis. 47 – 49


Ever since the discovery of microbes (they were first seen in the human mouth), we’ve known that the majority of bacteria that occur on our body are not harmful. However, we didn’t know what they actually do—and the devastating consequences of pathogens have given our microbial buddies a bad rap. Modern research techniques are revealing the many and complex roles of our gut bacteria, and the potential consequences when the crosstalk between the human and microbial cells in our bodies gets out of balance. We are starting to see this knowledge translated in healthcare changes, but we still have a way to go before we fully understand how the microbes in our gut work together, and with the rest of our bodies, as a complex system that keeps us healthy, or makes us sick.