Gut flora consists of a complex of microorganism species that live in the digestive tracts of animals and is the largest reservoir of human flora. In this context gut is synonymous with intestinal, and flora with microbiota and microflora; the word microbiome is also in use. Gut flora's primary benefit to the host is the gleaning of energy from the fermentation of undigested carbohydrates and the subsequent absorption of short chain fatty acids. The most important of these are butyrates, metabolised by the colonic epithelium; propionates by the liver; and acetates by the muscle tissue. Intestinal bacteria also play a role in synthesizing vitamin B and vitamin K as well as metabolising bile acids, sterols and xenobiotics. 
The human body carries about 100 trillion microorganisms in its intestines, a number ten times greater than the total number of human cells in the body. The metabolic activities performed by these bacteria resemble those of an organ, leading some to liken gut bacteria to a "forgotten" organ. It is estimated that these gut flora have around a hundred times as many genes in aggregate as there are in the human genome.
Bacteria make up most of the flora in the colon and up to 60% of the dry mass of feces. Somewhere between 300 and 1000 different species live in the gut, with most estimates at about 500. However, it is probable that 99% of the bacteria come from about 30 or 40 species. Fungi and protozoa also make up a part of the gut flora, but little is known about their activities.
Research suggests that the relationship between gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship. Though people can survive without gut flora, the microorganisms perform a host of useful functions, such as fermenting unused energy substrates, training the immune system, preventing growth of harmful, pathogenic bacteria, regulating the development of the gut, producing vitamins for the host (such as biotin and vitamin K), and producing hormones to direct the host to store fats. However, in certain conditions, some species are thought to be capable of causing disease by producing infection or increasing cancer risk for the host.
Not all the species in the gut have been identified because most cannot be cultured, and identification is difficult. Populations of species vary widely among different individuals but stay fairly constant within an individual over time, even though some alterations may occur with changes in lifestyle, diet and age. An effort to better describe the microflora of the gut and other body locations has been initiated; see Human microbiome project. In 2009, scientists from INRA (France) highlighted the existence of a small number of species shared by all individuals constituting the human intestinal microbiota phylogenetic core.
Most bacteria belong to the genera Bacteroides, Clostridium, Fusobacterium, Eubacterium, Ruminococcus, Peptococcus, Peptostreptococcus, and Bifidobacterium. Other genera, such as Escherichia and Lactobacillus, are present to a lesser extent. Species from the genus Bacteroides alone constitute about 30% of all bacteria in the gut, suggesting that this genus is especially important in the functioning of the host.
Predicting a human gut microbiota 
With a series of experiments using gnotobiotic mice, Faith et al. demonstrated that it is possible to predict changes in the human gut microbiota. They reproduced a model human gut community of ten sequenced human gut bacteria in mice and followed changes in community composition in response to changes in host diet.
Using several diets with different concentrations of four ingredients, casein, corn oil, cornstarch, and sucrose, it is possible to feed a linear model to predict the abundance of each species as a function of diet. This model is able to predict 61% of population variation. Total community abundance (biomass) and the abundance of each community member can best be explained by changes in casein consumption. Seven of these species are positively correlated with the concentration of casein and the other three species are negatively correlated with casein concentration.
The scientists also studied some diets consisting of random combinations of human pureed baby food and administered these diets to the mice. In this way, the diets were closer to real human diets. Again, the linear model could predict the 60% of the variation in species abundance knowing the concentrations of the components of the diets.
It has been demonstrated that there are common patterns of microbiome composition evolution during life. Analysing bacterial V4 16S rRNA from 528 individuals of different ages and geographic origins,  demonstrated that the diversity of microbiota composition of the fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults. Interestingly, the maturation of microbiota into an adult-like configuration happens during the three first years of life. The metanogenomic analysis of fecal samples combined with the analysis of V4 16S rRNA allowed a detailed study of phylotypes and showed that although, there are not phylotypes being unique to adults or babies, phylotypes belonging to Bifidobacteria longum wich dominate breast fed babies, decline in proportional representation with increasing age.
The study also showed a high prevalence of enzymes involved in fermentation, methanogenesis and in the metabolism of arginine, glutamate, aspartate and lysine in adult microbiomes whereas in baby microbiomes predominate enzymes involved in the metabolism of cysteine and fermentation pathways.
Finally, analysing the effects of kinship on the microbiome across countries, it has been found that despite the large influence of cultural factors on which microbes are present in the population, sharing numerous common environmental exposures in a family is a strong determinant of individual microbiome composition. This effect has no genetic influence and it is consistently observed in culturally different populations.
Gut flora and diet 
Studies and statistical analyses have identified the different bacterial genera in gut microbiota and their association with nutrient intake. Gut microflora is mainly composed by three enterotypes: Prevotella, Bacteroides and Ruminococcus. There is an association between the concentration of each microbial community and dietary components. For example, Prevotella is related with carbohydrates and simple sugars, indicating an association with a carbohydrate-based diet more typical of agrarian societies, while Bacteroides enterotypes is associated with animal proteins, aminoacids and saturated fats, components typical of a Western diet. That means that one enterotype will dominate over the other depending on the diet - those who eat plenty of protein and animal fats have predominantly Bacteroides bacteria, while for those who consume more carbohydrates the Prevotella species dominate.
Gut microbiome however can also be changed by following a long-term diet. People whose microbiome is predominantly Bacteroides (diet based on high levels of protein and fat) and change their dietary patterns to a diet based on high levels of carbohydrates, will get a Prevotella enterotype in the long-term. This relation may be interesting in medical field as the long term dietary interventions may allow modulation of an individual's enterotype to improve health.
Gut microbiome composition depends on the geographic origin of populations. Variations in trade off of Prevotella, the representation of the Urease gene, and the representation of genes encoding glutamate synthase/degradation or other enzymes involved in amino acids degradation or vitamin biosynthesis show significant differences between populations from USA, Malawi or Amerindian origin.
US population has a high representation of enzymes encoding the degradation of glutamine and enzymes involved in vitamin and lipoic acid biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of α-amylase in their microbiomes. As US populations have a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably a main determinant of gut bacterial compositon. 
Acquisition of gut flora in human infants 
The gastrointestinal tract of a normal fetus is sterile. During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. Immediately after vaginal delivery, babies may have bacterial strains derived from the mothers' feces in the upper gastrointestinal tract. Infants born by caesarean section may also be exposed to their mothers' microflora, but the initial exposure is most likely to be from the surrounding environment such as the air, other infants, and the nursing staff, which serve as vectors for transfer. The primary gut flora in infants born by caesarean delivery may be disturbed for up to six months after birth, whereas vaginally born infants take up to one month for their intestinal microflora to be well established. After birth, environmental, oral and cutaneous bacteria are readily transferred from the mother to the infant through suckling, kissing, and caressing. All infants are initially colonized by large numbers of E. coli and streptococci. Within a few days, bacterial numbers reach 108 to 1010 per gram of feces. During the first week of life, these bacteria create a reducing environment favorable for the subsequent bacterial succession of strict anaerobic species mainly belonging to the genera Bifidobacterium, Bacteroides, Clostridium, and Ruminococcus. Breast-fed babies become dominated by bifidobacteria, possibly due to the contents of bifidobacterial growth factors in breast milk. In contrast, the microbiota of formula-fed infants is more diverse, with high numbers of Enterobacteriaceae, enterococci, bifidobacteria, Bacteroides, and clostridia.
Baby microbiomes are enriched by enzymes involved in foraging of glycan represented in breast milk and the intestinal glucose.
Bacteria in the gut fulfill a host of useful functions for humans, including digestion of unutilized energy substrates, stimulating cell growth, repressing the growth of harmful microorganisms, training the immune system to respond only to pathogens, and defending against some diseases.
Carbohydrate fermentation and absorption 
Without gut flora, the human body would be unable to utilize some of the undigested carbohydrates it consumes, because some types of gut flora have enzymes that human cells lack for breaking down certain polysaccharides. Rodents raised in a sterile environment and lacking in gut flora need to eat 30% more calories just to remain the same weight as their normal counterparts. Carbohydrates that humans cannot digest without bacterial help include certain starches, fiber, oligosaccharides and sugars that the body failed to digest and absorb like lactose in the case of lactose intolerance and sugar alcohols, mucus produced by the gut, and proteins. A further result is flatulence, specifically due to the metabolism of oligosaccharides (notably from beans) by many different species.
Bacteria turn carbohydrates they ferment into short chain fatty acids (SCFAs) by a form of fermentation called saccharolytic fermentation. Products include acetic acid, propionic acid and butyric acid. These materials can be used by host cells, providing a major source of useful energy and nutrients for humans, as well as helping the body to absorb essential dietary minerals such as calcium, magnesium and iron. Gases and organic acids, such as lactic acid, are also produced by saccharolytic fermentation. Acetic acid is used by muscle, propionic acid helps the liver produce ATP, and butyric acid provides energy to gut cells and may prevent cancer. Evidence also indicates that bacteria enhance the absorption and storage of lipids and produce and then facilitate the body to absorb needed vitamins like vitamin K.
Another, less favorable type of fermentation, proteolytic fermentation, breaks down proteins like enzymes, dead host and bacterial cells, and collagen and elastin found in food, and can produce toxins and carcinogens in addition to SCFAs. Thus, a diet lower in protein reduces exposure to toxins.
Trophic effects 
Another benefit of SCFAs is that they increase growth of intestinal epithelial cells and control their proliferation and differentiation. They may also cause lymphoid tissue near the gut to grow. Bacterial cells also alter intestinal growth by changing the expression of cell surface proteins such as sodium/glucose transporters. In addition, changes they make to cells may prevent injury to the gut mucosa from occurring.
Repression of pathogenic microbial growth 
Another important role of helpful gut flora is that they prevent species that would harm the host from colonizing the gut through competitive exclusion, an activity termed the "barrier effect". Harmful yeasts and bacterial species such as Clostridium difficile (the overgrowth of which can cause pseudomembranous colitis) are unable to grow excessively due to competition from helpful gut flora species adhering to the mucosal lining of the intestine, thus animals without gut flora are infected very easily. The barrier effect protects humans from both invading species and species normally present in the gut at low numbers, whose growth is usually inhibited by the gut flora.
Helpful bacteria prevent the growth of pathogenic species by competing for nutrition and attachment sites to the epithelium of the colon. Symbiotic bacteria are more at home in this ecological niche and are thus more successful in the competition. Indigenous gut floras also produce bacteriocins, which are proteinaceous toxins that inhibit growth of similar bacterial strains, substances that kill harmful microbes and the levels of which can be regulated by enzymes produced by the host.
The process of fermentation, since it produces lactic acid and different fatty acids, also serves to lower the pH in the colon, preventing the proliferation of harmful species of bacteria and facilitating that of helpful species. The pH may also enhance the excretion of carcinogens.
Gut flora have a continuous and dynamic effect on the host's gut and systemic immune systems. The bacteria are key in promoting the early development of the gut's mucosal immune system both in terms of its physical components and function and continue to play a role later in life in its operation. The bacteria stimulate the lymphoid tissue associated with the gut mucosa to produce antibodies to pathogens. The immune system recognizes and fights harmful bacteria, but leaves the helpful species alone, a tolerance developed in infancy.
As soon as an infant is born, bacteria begin colonizing its digestive tract. The first bacteria to settle in are able to affect the immune response, making it more favorable to their own survival and less so to competing species; thus the first bacteria to colonize the gut are important in determining the person's lifelong gut flora makeup. However, there is a shift at the time of weaning from predominantly facultative anaerobic species, such as Streptococci and Escherichia coli, to mostly obligate anaerobic species.
Recent findings have shown that gut bacteria play a role in the expression of toll-like receptors (TLRs) in the intestines, molecules that help the host repair damage due to injury. TLRs cause parts of the immune system to repair injury caused, for example, by radiation. TLRs are one of the two classes of pattern-recognition receptors (PRR) that provide the intestine the ability to discriminate between the pathogenic and commensal bacteria. These PRRs identify the pathogens that have crossed the mucosal barriers and trigger a set of responses that take action against the pathogen, which involve three main immunosensory cells: surface enterocytes, M cells and dendritic cells.
The other class of PRRs are known as the nucleotide-binding oligomerization domain/caspase recruitment domain isoforms (NOD/CARD), which are cytoplasmic proteins that recognize endogenous or microbial molecules or stress responses and forms oligomers that activate inflammatory caspases. This would result in the cleavage and activation of important inflammatory cytokines and/or activate NF-κB signaling pathway to induce the production of inflammatory molecules.
Bacteria can influence the phenomenon known as oral tolerance, in which the immune system is less sensitive to an antigen (including those produced by gut bacteria) once it has been ingested. This tolerance, mediated in part by the gastrointestinal immune system and in part by the liver, can reduce an overreactive immune response like those found in allergies and auto-immune disease.
Some species of gut flora, such as some of those in the Bacteroides genus, are able to change their surface receptors to mimic those of host cells in order to evade immune response. Bacteria with neutral and harmful effects on the host can also use these types of strategies. The host immune system has also adapted to this activity, preventing overgrowth of harmful species.
Once the host immune system is developed, it regulates the bacterial composition in the gut. One of the regulation mechanisms is through the neutralizing action of secretory Immunoglobulin A (IgA) called immune exclusion Far beyond immune exclusion, IgAs are also essential to maintain the symbiotic balance between gut microbiota communities and the host immune system. Thus, there is a cross-talk between gut microbiota and the immune system which is basic for the production of the appropriate repertoire of IgA plasma cells. Kawamoto et al  have assessed the influence of the Inhibitory co receptor Programmed Cell Death 1 (PD-1) in this process. They observed that PD-1 deficiency generates an excess of T Follicular Helper Cells (TFH) with altered phenotypes, which results in deregulated selection of IgA precursor cells in the germinal center of Peyer’s patches. Consequently, the IgAs produced in PD-1-deficient mice have reduced bacteria-binding capacity, which causes alterations of microbial communities in the gut. Thus, PD-1 plays a critical role in the regulation of antibody diversification required for the maintenance of intact mucosal barrier.
The process is outlined in the figure as follows: Mature B cells production is activated by T Follicular Helpers (TFH), which are regulated by Programmed Cell Death Protein 1 (PD-1). Then, the selection of IgA determine the diversity of the antibody repertoire. Once inside the plasma cell, IgA dimer is produced from the interaction of IgA monomers with the Joining region (JR) and secreted to lamina propia. In addition to assembling monomeric IgA, the Joining chain (JR) interacts with the Polymeric immunoglobulin receptor (pIgR), an antibody-transporting protein expressed on the surface of mucosal epithelial cells, which contains Secretory IgA fragments. The polymeric immunoglobulin receptor transports IgA across epithelial cells. Next, on the one hand, the secretory IgA complex is translocated to the mucosal surface, where it will prevent commensal bacteria from breaching the mucosal surface . On the other hand, the IgA polymer leaves the epithelial cells, and will develop the immune exclusion.
Metabolic function 
The resident gut microflora positively control the intestinal epithelial cell differentiation and proliferation through the production of short-chain fatty acids. They also mediate other metabolic effects such as the syntheses of vitamins like biotin and folate, as well as absorption of ions including magnesium, calcium and iron.
The gut flora play a major role in metabolizing dietary carcinogens, the microcomponents and the macrocomponents. The microcomponents are genotoxic, and the major focus is on recent advances in heterocyclic amines (HCAs), which are produced by cooking at high temperatures proteinaceous food, such as meat and fish, which can then induce tumors in organs like the breast, colon and prostate. HCAs are naturally occurring; therefore, the complete avoidance of them is impractical, which is why the metabolic function of gut flora of such components is of great importance to the human, as this would help in prevention of such tumors that are difficult to avoid. The macrocomponents consists of the excessive intake of fat and sodium chloride, which can later promote tumors, such as in breasts and colons, from fat and gastric carcinogenesis from sodium chloride.
Preventing allergy 
Bacteria are also implicated in preventing allergies, an overreaction of the immune system to non-harmful antigens. Studies on the gut flora of infants and young children have shown that those who have or later develop allergies have different compositions of gut flora from those without allergies, with higher chances of having the harmful species C. difficile and S. aureus and lower prevalence of Bacteroides and Bifidobacteria. One explanation is that since helpful gut flora stimulate the immune system and "train" it to respond properly to antigens, a lack of these bacteria in early life leads to an inadequately trained immune system that overreacts to antigens. On the other hand, the differences in flora could be a result, not a cause, of the allergies.
Preventing inflammatory bowel disease 
Another indicator that bacteria help train the immune system is the epidemiology of Inflammatory Bowel Disease, or IBD, such as Crohn's Disease (CD). Some authors suggest that SCFAs prevent IBD. In addition, some forms of bacteria can prevent inflammation. The incidence and prevalence of IBD is high in industrialized countries with a high standard of living and low in less economically developed countries, having increased in developed countries throughout the twentieth century. The disease is also linked to good hygiene in youth; lack of breastfeeding; and consumption of large amounts of sucrose and animal fat. Its incidence is inversely linked with poor sanitation during the first years of life and consumption of fruits, vegetables, and unprocessed foods. Also, the use of antibiotics, which kill native gut flora and harmful infectious pathogens alike, especially during childhood, is associated with inflammatory bowel disease. On the other hand, using high concentrations of probiotics called "Amanlac" probiotics, helps to effectively maintain intestinal homeostasis, while also treating intestinal inflammation in IBD.
Alterations in flora balance 
Many tests with colitis-susceptible mice (Il10-/-) show significantly increased levels of luminal Verrucomicrobia, Bacteroidetes and Proteobacteria. For example, inflammation promotes an E. coli proliferation.
Effects of antibiotic use 
Altering the numbers of gut bacteria, for example by taking broad-spectrum antibiotics, may affect the host's health and ability to digest food. People may take the drugs to cure bacterial illnesses or may unintentionally consume significant amounts of antibiotics by eating the meat of animals to which they were fed. Antibiotics can cause antibiotic-associated diarrhea (AAD) by irritating the bowel directly, changing the levels of gut flora, or allowing pathogenic bacteria to grow. Another harmful effect of antibiotics is the increase in numbers of antibiotic-resistant bacteria found after their use, which, when they invade the host, cause illnesses that are difficult to treat with antibiotics.
Changing the numbers and species of gut flora can reduce the body's ability to ferment carbohydrates and metabolize bile acids and may cause diarrhea. Carbohydrates that are not broken down may absorb too much water and cause runny stools, or lack of SCFAs produced by gut flora could cause the diarrhea.
A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species such as C. difficile and Salmonella kedougou, and these species can get out of hand, though their overgrowth may be incidental and not be the true cause of diarrhea. Emerging treatment protocols for C. difficile infections involve fecal microbiota transplantation of donor feces. (see Fecal transplant). Initial reports of treatment describe success rates of 90%, with few side effects. Efficacy is speculated to result from restoring bacterial balances of bacteroides and firmicutes classes of bacteria.
Gut flora composition also changes in severe illnesses, due not only to antibiotic use but also to such factors as ischemia of the gut, failure to eat, and immune compromise. Negative effects from this have led to interest in selective digestive tract decontamination (SDD), a treatment to kill only pathogenic bacteria and allow the re-establishment of healthy ones.
Pharmabiotics is a generic term to encompass any form of therapeutic exploitation of the commensal flora, including the use of live probiotic bacteria, probiotic-derived biologically active metabolites, prebiotics, synbiotics or genetically modified commensal bacteria. Since the lack of gut flora can have such harmful health effects, the use of probiotics has anti-inflammatory effects in the gut and may be useful for improving health. Prebiotics are dietary components that can help foster the growth of micro-organisms in the gut, which may lead to better health. There is evidence supporting a therapeutic role for probiotic strategies for treating mucosal inflammatory disorders such as IBD, atopy, infection, diarrhoea, cancer and arthritis.
Women's gut microbiota change as pregnancy advances, with the changes similar to those seen in metabolic syndromes such as diabetes. The change in gut flora causes no ill effects. The newborn's gut biota resemble the mother's first-trimester samples. The diversity of the flora reduces from the first to third trimester, but the numbers of certain species go up.
Weight loss 
Weight loss initiates a shift in the bacteria phyla that compose gut flora. Specifically, Bacteroidetes increase nearly linearly as weight loss progresses.  While there is a high level of variation in bacteria species found among individual people, this trend is prominent and distinct in humans.
Role in disease 
Bacteria in the digestive tract have pathogenic properties in addition to their health-inducing ones: they can produce toxins and carcinogens and have been implicated in such conditions as multisystem organ failure, sepsis, colon cancer, and inflammatory bowel disease (IBD). A major factor in health is the balance of bacterial numbers; if the numbers grow too high or low, it will result in harm to the host. The host has enzymes to regulate this balance.
Some genera of bacteria, such as Bacteroides and Clostridium, have been associated with an increase in tumor growth rate, while other genera, such as Lactobacillus and Bifidobacteria, are known to prevent tumor formation.
Helpful bacteria can be very harmful to the host if they get outside of the intestinal tract. Translocation[disambiguation needed], which occurs when bacteria leave the gut through its mucosal lining, the border between the lumen of the gut and the inside of the body, can occur in a number of different diseases. It can be caused by too much growth of bacteria in the small intestine, reduced immunity of the host, or increased gut lining permeability. The gut can become more permeable in diseases like cirrhosis, which is damaging due in part to the activity of gut flora.
If the gut is perforated, bacteria can invade the body, causing a potentially fatal infection. Aerobic bacteria can make an infection worse by using up all available oxygen and creating an environment favorable to anaerobes.
Inflammatory bowel disease 
Some suspect that IBD is due to a reduction in immune tolerance and subsequent overreaction of the host's immune system to harmful or non-harmful bacteria. IBD may be caused by the entire gut flora together or some specific types.
It has been noted that though Ulcerative Colitis and Crohn's disease (two types of IBD) probably have genetic components, they are not inherited in a Mendelian fashion and are thus probably due to a complex set of factors rather than solely to a gene. Though neither bacterial colonization nor genetics is sufficient to cause the disease, bacteria probably play a role in these disorders.
Some suspect that inflammation in IBD is due to increased permeability of the inner lining of the colon, which may allow bacteria to invade the tissues and cause an immune reaction that leads to prolonged inflammation. Tissue damage in IBD results from the immunological misperception of danger within the naturally occurring flora or due to failure of normal tolerance to pathogenic bacteria. It is still unclear whether the inflammation that occurs is due to a specific subset of intestinal microbes or due to a problem with the tolerance of commensal gut flora. Abnormal tight junctions, which are supposed to prevent permeability, have been found in cells of patients with IBD. Because of the potentially harmful role of these bacteria, antibiotics are frequently prescribed to treat Crohn's disease. However, inflammation could occur first and cause the increased intestinal permeability found in diseases such as Crohn's, so the causative role of bacteria is not clear. Conventional therapies for IBD primarily target the mucosal inflammatory responses by using pharmabiotics.
It has been suggested that commensal bacteria are responsible for the development of colitis, since mice raised in a sterile environment do not get the disease. However, while some bacterial strains such as C. difficile and even normal gut bacteria cause colitis, others prevent the disease in mice.
Obese mice lacking leptin, a lipid metabolism regulator (ob/ob mice), have a distinct gut flora compared to (normal) lean mice, reflected in a change in the ratio between bacteria from the divisions Bacteroidetes and Firmicutes, which is shifted towards fewer Bacteroidetes and more Firmicutes in obese mice.
The microbes occupying the human gut are also in direct relation to obesity. A shift in the ratio between bacterial divisions Firmicutes and Bacteroidetes can be observed in lean and obese individuals—in the latter, a shift towards Firmicutes can be observed. The ratio between Firmicutes and Bacteroidetes dynamically reflects the overall weight condition of an individual, shifting towards Bacteroidetes if an obese individual loses weight.
The mutual influence of gut flora composition and weight condition is connected to differences in the energy-reabsorbing potential of different ratios of Firmicutes and Bacteroidetes, especially in the digestion of fatty acids and dietary polysaccharides, as shown by experiments wherein the (caecum) gut flora of obese mice were transplanted into germ-free recipient mice, leading to an increase in weight despite a decrease in food consumption.
See also 
- Helminthic therapy
- List of human flora
- Segmented filamentous bacteria
- Skin flora
Sources and notes 
- Cummings, J.H.; MacFarlane, G.T. (1997). "Role of intestinal bacteria in nutrient metabolism". Clinical Nutrition 16: 3–9. doi:10.1016/S0261-5614(97)80252-X. PMID 16844615.
- Björkstén B, Sepp E, Julge K, Voor T, Mikelsaar M (October 2001). "Allergy development and the intestinal microflora during the first year of life". J. Allergy Clin. Immunol. 108 (4): 516–20. doi:10.1067/mai.2001.118130. PMID 11590374.
- Guarner F, Malagelada JR (February 2003). "Gut flora in health and disease". Lancet 361 (9356): 512–9. doi:10.1016/S0140-6736(03)12489-0. PMID 12583961.
- Sears CL (October 2005). "A dynamic partnership: celebrating our gut flora". Anaerobe 11 (5): 247–51. doi:10.1016/j.anaerobe.2005.05.001. PMID 16701579.
- Steinhoff U (June 2005). "Who controls the crowd? New findings and old questions about the intestinal microflora". Immunol Lett 99 (1): 12–6. doi:10.1016/j.imlet.2004.12.013. PMID 15894105.
- Savage DC (1977). "Microbial ecology of the gastrointestinal tract". Annual Review of Microbiology 31: 107–133. doi:10.1146/annurev.mi.31.100177.000543. PMID 334036.
- O'Hara AM, Shanahan F (July 2006). "The gut flora as a forgotten organ". EMBO Rep. 7 (7): 688–93. doi:10.1038/sj.embor.7400731. PMC 1500832. PMID 16819463.
- Junjie Qin; et al (2009). "A human gut microbial gene catalogue established by metagenomic sequencing". Nature 464 (7285): 59–65. doi:10.1038/nature08821. PMID 20203603. Retrieved 2010-03-06
- University of Glasgow. 2005. The normal gut flora. Available through web archive. Accessed May 22, 2008[dead link]
- Stephen AM, Cummings JH (February 1980). "The microbial contribution to human faecal mass". J Med Microbiol 13 (1): 45–56. doi:10.1099/00222615-13-1-45. PMID 7359576.
- Gibson RG (2004). "Fibre and effects on probiotics (the prebiotic concept)". Clinical Nutrition Supplements 1 (2): 25–31. doi:10.1016/j.clnu.2004.09.005.
- Beaugerie L, Petit JC (April 2004). "Microbial-gut interactions in health and disease. Antibiotic-associated diarrhoea". Best Pract Res Clin Gastroenterol 18 (2): 337–52. doi:10.1016/j.bpg.2003.10.002. PMID 15123074.
- Vedantam G, Hecht DW (October 2003). "Antibiotics and anaerobes of gut origin". Curr. Opin. Microbiol. 6 (5): 457–61. doi:10.1016/j.mib.2003.09.006. PMID 14572537.
- Shanahan F (December 2002). "The host-microbe interface within the gut". Best Pract Res Clin Gastroenterol 16 (6): 915–31. doi:10.1053/bega.2002.0342. PMID 12473298.
- Tap J, Mondot S, Levenez F, Pelletier E, Caron C, Furet JP, Ugarte E, Muñoz-Tamayo R, Paslier DL, Nalin R, Dore J, Leclerc M (2009). "Towards the human intestinal microbiota phylogenetic core". Env. Microbiol. 11 (10): 2574–2584. doi:10.1111/j.1462-2920.2009.01982.x. PMID 19601958.
- Zimmer, Carl (April 20, 2011). "Bacteria Divide People Into 3 Types, Scientists Say". The New York Times. Retrieved April 21, 2011. "a group of scientists now report just three distinct ecosystems in the guts of people they have studied."
- Arumugam, Manimozhiyan; et al (March 2010). "Enterotypes of the human gut microbiome". Nature 473 (7346): 174–80. doi:10.1038/nature09944. PMID 21508958. "Our knowledge of species and functional composition of the human gut microbiome is rapidly increasing, but it is still based on very few cohorts and little is known about variation across the world. By combining 22 newly sequenced faecal metagenomes of individuals from four countries with previously published data sets, here we identify three robust clusters (referred to as enterotypes hereafter) that are not nation or continent specific."
- Faith, J. J.; McNulty, N. P.; Rey, F. E.; Gordon, J. I. (19 May 2011). "Predicting a Human Gut Microbiota's Response to Diet in Gnotobiotic Mice". Science 333 (6038): 101–4. doi:10.1126/science.1206025.
- Tanya Yatsunenko & Jeffrey I.Gordon et al.(2012) " Human gut microbiome viewed across age and geography" Nature 486 (11053): 222-228.
- Wu, G.D., et al.; Chen; Hoffmann; Bittinger; Chen; Keilbaugh; Bewtra; Knights et al. (2011). "Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes". Science 334 (6052): 105–108. Bibcode:2011Sci...334..105W. doi:10.1126/science.1208344. PMC 3368382. PMID 21885731.
- Tanya Yatsunenko & Jeffrey I.Gordon et al.(2012) " Human gut microbiome viewed across age and geography" Nature 486 (11053): 222-228.
- Bettelheim KA, Breadon A, Faiers MC, O'Farrell SM, Shooter RA (February 1974). "The origin of O serotypes of Escherichia coli in babies after normal delivery". J Hyg (Lond) 72 (1): 67–70. doi:10.1017/S0022172400023226. PMC 2130250. PMID 4593741.
- Schwiertz A, Gruhl B, Löbnitz M, Michel P, Radke M, Blaut M (September 2003). "Development of the intestinal bacterial composition in hospitalized preterm infants in comparison with breast-fed, full-term infants". Pediatr. Res. 54 (3): 393–9. doi:10.1203/01.PDR.0000078274.74607.7A. PMID 12788986.
- Fecal Microflora in Healthy Infants Born by Different Methods of Delivery: Permanent Changes in Intestinal Flora After Cesarean Delivery Grölund, Minna-Maija*†; Lehtonen, Olli-Pekka†; Eerola, Erkki‡; Kero, Pentti*Journal of Pediatric Gastroenterology & Nutrition: January 1999 - Volume 28 - Issue 1 - pp 19-25
- Mackie RI, Sghir A, Gaskins HR (1 May 1999). "Developmental microbial ecology of the neonatal gastrointestinal tract". Am. J. Clin. Nutr. 69 (5): 1035S–1045S. PMID 10232646.
- Favier CF, Vaughan EE, De Vos WM, Akkermans AD (January 2002). "Molecular Monitoring of Succession of Bacterial Communities in Human Neonates". Appl. Environ. Microbiol. 68 (1): 219–26. doi:10.1128/AEM.68.1.219-226.2002. PMC 126580. PMID 11772630.
- Coppa GV, Bruni S, Morelli L, Soldi S, Gabrielli O (July 2004). "The first prebiotics in humans: human milk oligosaccharides". J. Clin. Gastroenterol. 38 (6 Suppl): S80–3. doi:10.1097/01.mcg.0000128926.14285.25. PMID 15220665.
- Coppa GV, Zampini L, Galeazzi T, Gabrielli O (Dec 2006). "Prebiotics in human milk: a review". Dig Liver Dis. 38 (6 Suppl 2): S80–3. doi:10.1016/S1590-8658(07)60013-9. PMID 17259094.
- Harmsen HJ, Wildeboer-Veloo AC, Raangs GC, et al. (January 2000). "Analysis of intestinal flora development in breast-fed and formula-fed infants by using molecular identification and detection methods". J. Pediatr. Gastroenterol. Nutr. 30 (1): 61–7. doi:10.1097/00005176-200001000-00019. PMID 10630441.
- Fanaro S, Chierici R, Guerrini P, Vigi V (September 2003). "Intestinal microflora in early infancy: composition and development". Acta Paediatr Suppl 91 (441): 48–55. PMID 14599042.
- Wynne AG, McCartney AL, Brostoff J, Hudspith BN, Gibson GR (June 2004). "An in vitro assessment of the effects of broad-spectrum antibiotics on the human gut microflora and concomitant isolation of a Lactobacillus plantarum with anti-Candida activities". Anaerobe 10 (3): 165–9. doi:10.1016/j.anaerobe.2004.03.002. PMID 16701514.
- Keeley J. 2004. Good bacteria trigger proteins to protect the gut. Howard Hughes Medical Institute. EurekAlert. Accessed January 9, 2007.
- Jewell AP (2005). "Is the liver an important site for the development of immune tolerance to tumours?". Med. Hypotheses 64 (4): 751–4. doi:10.1016/j.mehy.2004.10.002. PMID 15694692.
- “Mantis N.J., Rol N., Corthésy B. Secretory IgA’s complex roles in immunity and mucosal homeostasis in the gut. 2011. Mucosal Immunol. , 4 (6): 603-11”
- “The Inhibitory Receptor PD-1 Regulates IgA Selection and Bacterial Composition in the Gut Shimpei Kawamoto et al. Science 336, 485 (2012); DOI: 10.1126/science.1217718”
- Sugimura T (March 2000). "Nutrition and dietary carcinogens". Carcinogenesis 21 (3): 387–95. doi:10.1093/carcin/21.3.387. PMID 10688859.
- Guarner F, Malagelada JR (October 2003). "Role of bacteria in experimental colitis". Best Pract Res Clin Gastroenterol 17 (5): 793–804. doi:10.1016/S1521-6918(03)00068-4. PMID 14507589.
- Hahm Ki Baik, et al. "High Concentrated Probiotics Improve Inflammatory Bowel Diseases Better Than Commercial Concentration Of Probiotics." Journal Of Food & Drug Analysis 20.(2012): 292-295. Academic Search Premier.
- Carman RJ, Simon MA, Fernández H, Miller MA, Bartholomew MJ (December 2004). "Ciprofloxacin at low levels disrupts colonization resistance of human fecal microflora growing in chemostats". Regul. Toxicol. Pharmacol. 40 (3): 319–26. doi:10.1016/j.yrtph.2004.08.005. PMID 15546686.
- Brandt Lawrence J. MD (September 2011). "Endoscopic Fecal Microbiota Transplantation: "First-Line" Treatment for Severe Clostridium difficile Infection?". Journal of Clinical Gastroenterology 45 (8): 655–7. doi:10.1097/MCG.0b013e3182257d4f. PMID 21716124.
- Knight DJ, Girling KJ (May 2003). "Gut flora in health and disease". Lancet 361 (9371): 1831. doi:10.1016/S0140-6736(03)13438-1. PMID 12781578.
- Monya Baker (August 2, 2012). "Pregnancy alters resident gut microbes". Nature News. doi:10.1038/nature.2012.11118.
- RE Ley; et al (2006). "Human gut microbes associated with obesity". Nature 441 (7122): 21–28
- GL Hold; et al (2002). "Assessment of microbial diversity in human colonic samples by 16S rDNA sequence analysis". FEMS Microbiol Ecol 39 (1): 33–39. doi:10.1111/j.1574-6941.2002.tb00904.x. PMID 19709182
- Suenaert P, Bulteel V, Lemmens L, et al. (August 2002). "Anti-tumor necrosis factor treatment restores the gut barrier in Crohn's disease". Am. J. Gastroenterol. 97 (8): 2000–4. doi:10.1111/j.1572-0241.2002.05914.x. PMID 12190167.
- Garcia-Tsao G, Wiest R (April 2004). "Gut microflora in the pathogenesis of the complications of cirrhosis". Best Pract Res Clin Gastroenterol 18 (2): 353–72. doi:10.1016/j.bpg.2003.10.005. PMID 15123075.
- Hugot JP (June 2004). "Inflammatory bowel disease: a complex group of genetic disorders". Best Pract Res Clin Gastroenterol 18 (3): 451–62. doi:10.1016/j.bpg.2004.01.001. PMID 15157820.
- Veltkamp C, Tonkonogy SL, De Jong YP, et al. (March 2001). "Continuous stimulation by normal luminal bacteria is essential for the development and perpetuation of colitis in Tg(epsilon26) mice". Gastroenterology 120 (4): 900–13. doi:10.1053/gast.2001.22547. PMID 11231944.
- Ley RE, Turnbaugh PJ, Klein S, Gordon JI (December 2006). "Microbial ecology: human gut microbes associated with obesity". Nature 444 (7122): 1022–3. doi:10.1038/4441022a. PMID 17183309.
- Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI (December 2006). "An obesity-associated gut microbiome with increased capacity for energy harvest". Nature 444 (7122): 1027–31. doi:10.1038/nature05414. PMID 17183312.
- Bäckhed F, Manchester JK, Semenkovich CF, Gordon JI (January 2007). "Mechanisms underlying the resistance to diet-induced obesity in germ-free mice". Proc. Natl. Acad. Sci. U.S.A. 104 (3): 979–84. doi:10.1073/pnas.0605374104. PMC 1764762. PMID 17210919.
- Bäckhed F, Ding H, Wang T, et al. (November 2004). "The gut microbiota as an environmental factor that regulates fat storage". Proc. Natl. Acad. Sci. U.S.A. 101 (44): 15718–23. doi:10.1073/pnas.0407076101. PMC 524219. PMID 15505215.
Further reading 
- Hattner, J.A.T./Anderes, S. ”Gut Insight: probiotics and prebiotics for digestive health and well-being”, 2009, Hattner Nutrition. ISBN 978-0-578-02615-2
- Review articles
- Prakash, S. et al. “The Gut Microbiota and Human Health with an Emphasis on the Use of Microencapsulated Bacterial Cells”, Journal of Biomedicine and Biotechnology (2011),
- De Preter, V. et al. ”The impact of pre- and/or probiotics on human colonic metabolism: Does it affect human health?”, Molecular Nutrition & Food Research (2011),55(1):46-57.
- Prakash, S. et al. “Gut microbiota: next frontier in understanding human health and development of biotherapeutics”, Biologics: Targets & Therapy (2011), 5:71-86.
- Wu, G.D. et al. "Linking Long-Term Dietary Patterns with Gut Microbial Enterotypes", Science 7 October 2011. Vol 334 pag 105-108.
- International Human Microbiome Consortium
- International Probiotics Association
- International Scientific Association for Probiotics and Prebiotics
- Isabelle Moncada; Mario Fossati; Ventura Samarra (23 January 2013). "Microbiote : ces bactéries qui nous gouvernent" (video). 36.9° (fr) (in French) (Geneva, Switzerland: Radio télévision suisse). Retrieved 26 January 2013. Les scientifiques viennent de découvrir un nouvel organe. Un organe non pas composé de cellules humaines, mais de bactéries. Cette découverte bouleverse la perception que l'on avait du corps humain et ouvre la porte à la compréhension de maladies a priori aussi éloignées l'une de l'autre que l'obésité et l'autisme.