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Original- "Human microbiota"

The gut flora has the largest numbers of bacteria and the greatest number of species compared to other areas of the body.[1] In humans the gut flora is established at one to two years after birth, and by that time the intestinal epithelium and the intestinal mucosal barrier that it secretes have co-developed in a way that is tolerant to, and even supportive of, the gut flora and that also provides a barrier to pathogenic organisms.[2][3]

The relationship between some gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship.[4] Some human gut microorganisms benefit the host by fermentating dietary fiber into short-chain fatty acids (SCFAs), such as acetic acid and butyric acid, which are then absorbed by the host.[1][5] Intestinal bacteria also play a role in synthesizing vitamin B and vitamin K as well as metabolizing bile acids, sterols, and xenobiotics.[4][5] The systemic importance of the SCFAs and other compounds they produce are like hormones and the gut flora itself appears to function like an endocrine organ,[5] and dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions.[1][6]

The composition of human gut flora changes over time, when the diet changes, and as overall health changes.[1][6] A systematic review of 15 human randomized controlled trials from July 2016 found that certain commercially available strains of probiotic bacteria from the Bifidobacterium and Lactobacillus genera (B. longum, B. breve, B. infantis, L. helveticus, L. rhamnosus, L. plantarum, and L. casei), when taken by mouth in daily doses of 109–1010 colony forming units (CFU) for 1–2 months, possess treatment efficacy (i.e., improved behavioral outcomes) in certain central nervous system disorders – including anxiety, depression, autism spectrum disorder, and obsessive–compulsive disorder – and improved certain aspects of memory.[7]


Edit- "Human microbiota"

The gut flora has the largest numbers of bacteria and the greatest number of species compared to other areas of the body.[1] In humans the composition of gut flora is established during birth.[8] Birth by Cesarean section or vaginal delivery also influences the gut's microbial composition. Babies born through the vaginal canal have non-pathogenic, beneficial gut microbiota similar to those found in the mother.[9] However, the gut microbiota of babies delivered by C-section harbors more pathogenic bacteria such as Escherichia coli and Staphylococcus and it takes longer to develop non-pathogenic, beneficial gut microbiota.[10]

The relationship between some gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship.[4] Some human gut microorganisms benefit the host by fermentating dietary fiber into short-chain fatty acids (SCFAs), such as acetic acid and butyric acid, which are then absorbed by the host.[1][5] Intestinal bacteria also play a role in synthesizing vitamin B and vitamin K as well as metabolizing bile acids, sterols, and xenobiotics.[4][5] The systemic importance of the SCFAs and other compounds they produce are like hormones and the gut flora itself appears to function like an endocrine organ,[5] and dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions.[1][6]

The composition of human gut flora changes over time, when the diet changes, and as overall health changes.[1][6] A systematic review of 15 human randomized controlled trials from July 2016 found that certain commercially available strains of probiotic bacteria from the Bifidobacterium and Lactobacillus genera (B. longum, B. breve, B. infantis, L. helveticus, L. rhamnosus, L. plantarum, and L. casei), when taken by mouth in daily doses of 109–1010 colony forming units (CFU) for 1–2 months, possess treatment efficacy (i.e., improved behavioral outcomes) in certain central nervous system disorders – including anxiety, depression, autism spectrum disorder, and obsessive–compulsive disorder – and improved certain aspects of memory.[7]. However, changes in the composition of gut microbiota has also been found to be correlated with harmful effects on health. In an article published by Musso et al., it was found that the gut microbiota of obese invidividuals had more Firmicutes and less Bacteroidetes than healthy individuals.[11] Furthermore, a study done by Gordon et al., confirmed that it was the composition of the microbiota that causes obesity rather than the other way around. This was done by transplanting the gut microbiota from diet-induced obese(DIO) mice or lean control mice into lean germ-free mice that do not have a microbiome. They found that the mice transplanted with DIO mouse gut microbiota had significantly higher total body fat than the mice transplanted with lean mouse microbiota when given the same diet.[12] Cheng Xi (talk) 02:24, 9 October 2017 (UTC)

  1. ^ a b c d e f g h Cite error: The named reference Quigley2013rev was invoked but never defined (see the help page).
  2. ^ Sommer, F; Bäckhed, F (Apr 2013). "The gut microbiota--masters of host development and physiology". Nat Rev Microbiol. 11 (4): 227–38. doi:10.1038/nrmicro2974. PMID 23435359. S2CID 22798964.
  3. ^ Faderl, M; et al. (Apr 2015). "Keeping bugs in check: The mucus layer as a critical component in maintaining intestinal homeostasis". IUBMB Life. 67 (4): 275–85. doi:10.1002/iub.1374. PMID 25914114. S2CID 25878594. {{cite journal}}: Explicit use of et al. in: |last2= (help)
  4. ^ a b c d Cite error: The named reference Prescotts was invoked but never defined (see the help page).
  5. ^ a b c d e f Clarke, G; et al. (Aug 2014). "Minireview: Gut microbiota: the neglected endocrine organ". Mol Endocrinol. 28 (8): 1221–38. doi:10.1210/me.2014-1108. PMC 5414803. PMID 24892638. {{cite journal}}: Explicit use of et al. in: |last2= (help)
  6. ^ a b c d Shen S, Wong CH. "Bugging inflammation: role of the gut microbiota. Clin Transl Immunology. 2016 Apr;5(4):e72. Review. doi:10.1038/cti.2016.12 PMID 27195115 PDF
  7. ^ a b Wang H, Lee IS, Braun C, Enck P (July 2016). "Effect of probiotics on central nervous system functions in animals and humans - a systematic review". J. Neurogastroenterol Motil. 22 (4): 589–605. doi:10.5056/jnm16018. PMC 5056568. PMID 27413138. These probiotics showed efficacy in improving psychiatric disorder-related behaviors including anxiety, depression, autism spectrum disorder (ASD), obsessive-compulsive disorder, and memory abilities, including spatial and non-spatial memory. Because many of the basic science studies showed some efficacy of probiotics on central nervous system function, this background may guide and promote further preclinical and clinical studies. ... According to the qualitative analyses of current studies, we can provisionally draw the conclusion that B. longum, B. breve, B. infantis, L. helveticus, L. rhamnosus, L. plantarum, and L. casei were most effective in improving CNS function, including psychiatric disease-associated functions (anxiety, depression, mood, stress response) and memory abilities
  8. ^ Yang, Irene; Corwin, Elizabeth J.; Brennan, Patricia A.; Jordan, Sheila; Murphy, Jordan R.; Dunlop, Anne (2016). "The Infant Microbiome". Nursing Research. 65 (1): 76–88. doi:10.1097/NNR.0000000000000133. S2CID 11411986.
  9. ^ Mueller, Noel T.; Bakacs, Elizabeth; Combellick, Joan; Grigoryan, Zoya; Dominguez-Bello, Maria G. (February 2015). "The infant microbiome development: mom matters". Trends in Molecular Medicine. 21 (2): 109–117. doi:10.1016/j.molmed.2014.12.002. PMC 4464665. PMID 25578246.
  10. ^ Wall, R; Ross, R.P; Ryan, C.A; Hussey, S; Murphy, B; Fitzgerald, G.F; Stanton, C (4 March 2009). "Role of Gut Microbiota in Early Infant Development". Clinical Medicine. Pediatrics. 3: 45–54. doi:10.4137/cmped.s2008. ISSN 1178-220X. PMC 3676293. PMID 23818794.
  11. ^ Musso, G.; Gambino, R.; Cassader, M. (28 September 2010). "Obesity, Diabetes, and Gut Microbiota: The hygiene hypothesis expanded?". Diabetes Care. 33 (10): 2277–2284. doi:10.2337/dc10-0556. S2CID 207364861.
  12. ^ Turnbaugh, Peter J.; Bäckhed, Fredrik; Fulton, Lucinda; Gordon, Jeffrey I. (April 2008). "Diet-Induced Obesity Is Linked to Marked but Reversible Alterations in the Mouse Distal Gut Microbiome". Cell Host & Microbe. 3 (4): 213–223. doi:10.1016/j.chom.2008.02.015. PMC 3687783. PMID 18407065.
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