Table of contentsIntroductionFunctions of the gut microbiotaDysbiosis and diseasesIntroductionRecent studies have allowed us to conclude that we are super-organisms in which microbial symbionts play essential physiological functions. The human microbiome has become the crucial moderator of interactions between food and our bodies and can alter our state of mind and health or play a central role in a wide range of diseases. There are currently 52 recognized bacterial phyla on Earth, 5 to 7 of which reside in the gastrointestinal tract which is home to over 100 trillion bacteria. Firmicutes, Bacteroidetes and Actinobacteria are the 3 major phyla to which most of the gastrointestinal microbiota belongs. In my self-study essay, I will talk about the importance of the gut microbiota and the role it plays in host health as well as the potential links it has with certain diseases. First, let's talk about the multiple functions of the microbiota in the immune and nervous systems, as well as its role in metabolism, homeostasis, and protection against pathobiont overgrowth. I will then continue by mentioning the potential link they may have with the following diseases: obesity, colorectal cancer, Clostridium difficile infection and inflammatory bowel disease. I will conclude with my personal opinion on the subject and possible future perspectives and research that needs to be conducted. Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay Functions of the Gut Microbiota The gut microbiota has a major role to play in immune, neuroendocrine, and metabolic interactions that stabilize and regulate their symbiotic relationship with the host. .1) Immunity and nervous system: The intestinal barrier protects the internal environment of the host from the external environment and consists of the epithelial and mucous layers. Disruption of its function increases intestinal permeability to commensal microbes and their products and leads to aberrant immunoinflammatory responses such as inflammation, allergy and autoimmune disease, controlled by a dysregulated T cell response and a molecular mimicry. The gut microbiota cross-regulates the physical and immunological functions of the intestinal barrier. Tight regulation of the gastrointestinal T cell balance, such as the Treg/TH17 balance, is vital to maintain intestinal homeostasis and prevent an aberrant immunoinflammatory response. Recent studies have shown that the gut microbiota has a role to play in the regulation of the host immune response and in immunity at local and systemic levels. Studies in germ-free mice have indicated that the gut microbiota facilitates the maturation of lymphocytopoiesis and hematopoiesis, as well as adaptive and innate immunity. The host microbiota and their SCFAs (short-chain fatty acids), also regulate the maturation and functionality of microglia, which are the tissue macrophages of the central nervous system (CNS) [8], they also play a massive role in maintaining microglia homeostasis which is crucial for maintaining CNS health. The gut microbiota also plays a modulatory role in the enteric nervous system (ENS), which communicates bidirectionally with the CNS to form the gut-brain axis by autonomously regulating the physiology and function of the gastrointestinal tract. Enteric glial cells (EGCs) constitute the main component of the ENS. They form the enteric glial network andregulate functions such as intestinal motility, immuno-inflammatory reactions, blood flow and endocrine/exocrine reactions. Various gastrointestinal disorders such as IBD, infection-induced intestinal inflammation, neurodegenerative disorders, and motility disorders have all been associated with dysfunctions of the ENS and EGC. Recent studies have shown that the close proximity of the gut microbiota and the ENS throughout the gastrointestinal tract allows them to modulate the functioning and development of the ENS. Studies on germ-free mice have shown a notable decrease in intestinal motility compared to mice without specific pathogen and modified counterparts of the Schaedler flora and highlight the importance of the play of the intestinal microbiota in the postnatal development of the ENS in the mid to distal intestine. Finally, toll-like receptors (TLRs) play an essential role in maintaining intestinal homeostasis and the symbiotic relationship between the host and the intestinal microbiota. . Expression of TLR4 possibly endows the ENS with the ability to respond instantly to stimuli derived from the gut microbiota, suggesting that TLRs may be the link between the gut microbiota and the development of the ENS. All of the points above highlight that the gut microbiota has a large number of roles to play in the immune and nervous systems. 2) Metabolism: The gut microbiota facilitates host energy recovery and metabolic efficiency through enrichment of the metabolism of amino acids, polysaccharides, micronutrients and xenobiotics. revealed from human fecal samples using metagenomic and 16S ribosomal RNA sequencing techniques. Fermentation of unabsorbed starch and soluble dietary fiber is another important role of the gut microbiota, with the final product in the form of SCFAs which act as one of the energy substrates for the host and contribute to an additional 10% daily intake of dietary energy for other metabolisms. process. SCFAs regulate energy homeostasis by stimulating GPR41-mediated leptin production. Studies in mice have shown a link between interactive host-microbe signaling and immune-inflammatory crosstalk of the gut-brain axis, as leptin exhibits pleiotropic effects on physiological functions such as appetite and energy metabolism , as well as on the immune response and sympathetic nervous activity. Gut microbes also synthesize vitamins. which are micronutrients that have beneficial value for microbial and host metabolism. Vitamin K-producing gut bacteria (e.g. Bacteroides fragilis) anaerobically synthesize vitamin K2 which helps reduce the risk of cardiovascular disorders such as coronary heart disease, by decreasing vascular calcification, lowering cholesterol levels and raising HDL. The intestinal microbiota also exclusively synthesizes vitamins B5 and B12 which act as coenzymes for the production of cortisol and acetylcholine essential for the proper functioning of the nervous system. Neuropsychological and hermatogic disorders as well as insomnia and gastrointestinal discomfort have all been associated with vitamin B5 and B12 deficiencies. The gut microbiota also plays an important role in the cometabolism of bile acids, which facilitate digestion, as well as cholesterol and lipid metabolisms. In humans, 95% of bile acids are reabsorbed in the distal ileum. The 5% of unabsorbed primary bile acids become secondary bile acids by bioconversion or deconjugation by theBile acids secreted by the colonic microbiota. They are then partially reabsorbed in the colon and then brought back to the liver to be conjugated there. Unabsorbed secondary bile acids are excreted by the host. Primary and secondary bile acids serve to regulate bile acid production, glucose metabolism, and perhaps even hepatic autophagy, by activating host FXR signaling. Secondary bile acids can even protect the host against a range of infectious pathogens and help shape the composition of the gut microbiota using antimicrobial properties that alter the integrity of the microbial cell membrane to cause spillage of intracellular contents and inhibit the growth of microbes intolerant to bile acids.3) Protection against pathobionts: the human microbiota protects the host from the proliferation of pathogenic microbiota (pathobionts) using 2 mechanisms of action. Competition with pathogens for shared niches and nutrients, and suppression of the pathogen by enhancing the host defense mechanism. Dominant members of the non-pathogenic gut microbiota occupy the niche and suppress pathogen growth and colonization. A decrease in dominant members of the microbiota upon disruption of the gut microbiome allows opportunistic pathogenic strains to colonize empty niches and leads to infection. Dysbiosis and diseasesDysbiosis is an imbalance in the taxonomic composition of the gut microbiota and can be caused by external factors and by the host. External factors may include antibiotic consumption, diet and stress. Dysbiosis prevents the gut microbiota from maintaining host well-being and can result in an increase in the number of pathobionts, leading to unregulated production of products or metabolites of microbial origin that can be harmful to the host. host and cause various diseases on local, systemic or distant organs. In short, dysbiosis is the possible link between the gut microbiome and disease manifestation. 1) Obesity: Obesity is a global health risk and affects more than 600 million people worldwide. Obesity can be caused by a number of factors such as genetics, behavior and environmental factors and is linked to the gut microbiome through its function in regulating host metabolism. High energy intake and decreased energy expenditure are classic signs of obesity and are linked to metabolic syndrome, causing excessive fat accumulation and posing a higher risk of developing obesity-associated disorders, e.g. type 2 diabetes and premature mortality. The gut microbiota contributes to the development of obesity by facilitating increased digestion of food, leading to higher energy harvest and increased fat deposition, suppressing lipoprotein lipase inhibitors to store triacylglycerides in adipocytes and by promoting hepatic DNL through the expression of enzymes synthesizing hepatic fatty acids. Furthermore, increased endotoxic LPS of Gram-negative gut bacteria can lead to obesity-associated metabolic syndrome, obesity-associated insulin resistance, and low-grade inflammation. As seen in animal models, prebiotics or probiotics can be used through dietary intervention to selectively modulate microbial composition as a possible therapeutic approach for obesity-related metabolic disorders due to their association with dysbiosis of the intestinal microbiota. These arepromising treatments for the future but more clinical. further testing and data from human models are needed to prove their success.2) Clostridium Difficile Infection (CDI): Clostridium difficile is a Gram-positive toxin and spore-producing anaerobe and is a member of Firmicutes in the intestinal microbiota. CDI is a serious disease with 453,000 cases resulting in deaths in America in 2011 alone. Diarrhea, pseudomembranous colitis, sepsis, and mortality in severe cases are some of the symptoms associated with CDI. Antibiotic administration can be a major risk factor for CDI, with 5-35% of people developing diarrhea as a side effect. CDI used several modes of horizontal gene transfer within strains and possibly commensal microbes to acquire genes resistant to a number of antibiotics, including clindamycin, erythromycin, chloramphenicol, and linezolid. The exact mechanism of antibiotic-associated diarrhea remains unknown, but its correlation with CDI requires research into the link between C. difficile and the gut microbiome in a healthy state. The dominant gut microbiota is currently thought to protect the host from C. difficile overgrowth in the normal microbiome by using colonization resistance mechanisms. While researchers propose that primary bile acids serve as germinants for C. difficile spores and secondary bile acids inhibit the vegetative growth of C. difficile. Antibiotic administration reduces secondary bile acid diversity by disrupting intestinal microbial communities. This makes the host more susceptible to CDI, as there is a reduction in the bioconversion of primary bile acids to antimicrobial secondary bile acids, which leads to growth of C. difficile. Greater amounts of vegetative C. difficile lead to diarrhea because the secretion of toxins damages the intestinal barrier, stimulates a severe inflammatory response, and impairs ion absorption. Novel therapeutic treatments have been developed involving restoration of the gut microbiota through a better understanding of CDI and the role that antibiotic-induced microbiome dysbiosis must play in its pathogenesis. An example of such treatment is FMT, where gut microbiota from a healthy donor's stool is used to restore intestinal homeostasis and patients who received it showed a lasting elevation in fecal microbial diversity and a rate high recovery of 90% compared to vancomycin of 60%. While studies have shown patients who received FMT had a 94% cure rate from CDI, with no disease recurrence observed during 16-month follow-up. After receiving FMT, patients showed signs of increased beneficial bacteria and elevated plasma levels of the antimicrobial peptide LL-37 as well as a reduction in pro-inflammatory cytokines. Studies using FMT indicate a strong association between the gut microbiome and the development of CDI. Although more advanced studies need to be conducted in order to uncover the exact beneficial strains and underlying mechanisms of FMT, they hold great potential for the future and highlight the widespread use of microbiota shift therapy in the fight against CDI.4) Inflammatory bowel diseases (IBD): IBD is a group of idiopathic, multifactorial, persistent and recurrent gastrointestinal inflammations in two forms, CD and UC. In CD, inflammation can occur anywhere throughout the entire gastrointestinal tract, whereas UC is limited to the large.