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Development of enteric protection and immune system
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In humans, a gut flora similar to an adult's is formed within one to two years of birth.[1] As the gut flora gets established, the lining of the intestines – the intestinal epithelium and the intestinal mucosal barrier that it secretes – develop as well, in a way that is tolerant to, and even supportive of, commensurate microorganisms to a certain extent and also provides a barrier to pathogenic ones.[1][2]Specifically, goblet cells that produce the mucosa proliferate, and the mucosa layer thickens, providing an outside mucosal layer in which "friendly" microorganisms can anchor and feed, and an inner layer that even these organisms cannot penetrate.[1][2] Additionally, the development of gut-associated lymphoid tissue (GALT), which forms part of the intestinal epithelium and which detects and reacts to pathogens, appears and develops during the time that the gut flora develops and established.[1] The GALT that develops is tolerant to gut flora species, but not to other microorganisms.[1] GALT also normally becomes tolerant to food to which the infant is exposed, as well as digestive products of food, and gut flora's metabolites produced from food.[1]
The human immune system creates cytokines that can drive the immune system to produce inflammation in order to protect itself, and that can tamp down the immune response to maintain homeostasis and allow healing after insult or injury.[1] Different bacterial species that appear in gut flora have been shown to be able to drive the immune system to create cytokines selectively; for example Bacteroides fragilis and some Clostridia species appear to drive an anti-inflammatory response, while some segmented filamentous bacteria drive the production of inflammatory cytokines.[1][3] Gut flora can also regulate the production of antibodies by the immune system.[1][4] These cytokines and antibodies can have effects outside the gut, in the lungs and other tissues.[1]
Development of enteric protection and immune system
edit In humans, a gut flora similar to an adult's is formed within one to two years of birth.[1] As the gut flora gets established, the lining of the intestines – the intestinal epithelium and the intestinal mucosal barrier that it secretes – develop as well, in a way that is tolerant to, and even supportive of, commensurate microorganisms to a certain extent and also provides a barrier to pathogenic ones.[1] Specifically, goblet cells that produce the mucosa proliferate, and the mucosa layer thickens, providing an outside mucosal layer in which "friendly" microorganisms can anchor and feed, and an inner layer that even these organisms cannot penetrate.[1][2] Additionally, the development of gut-associated lymphoid tissue (GALT), which forms part of the intestinal epithelium and which detects and reacts to pathogens, appears and develops during the time that the gut flora develops and established.[1] The GALT that develops is tolerant to gut flora species, but not to other microorganisms.[1] GALT also normally becomes tolerant to food to which the infant is exposed, as well as digestive products of food, and gut flora's metabolites produced from food.[1]
The human immune system creates cytokines that can drive the immune system to produce inflammation in order to protect itself, and that can tamp down the immune response to maintain homeostasis and allow healing after insult or injury.[1] Different bacterial species that appear in gut flora have been shown to be able to drive the immune system to create cytokines selectively; for example Bacteroides fragilis and some Clostridia species appear to drive an anti-inflammatory response, while some segmented filamentous bacteria drive the production of inflammatory cytokines.[1][3] Gut flora can also regulate the production of antibodies by the immune system.[1][4] One function of this regulation is to cause B cells to class switch to IgA. In most cases B cells need activation from T helper cells to induce class switching; however, in another pathway, gut flora cause NF-kB signaling by intestinal epithelial cells which results in further signaling molecules being secreted[5]. These signaling molecules interact with B cells to induce class switching to IgA [5]. IgA is an important type of antibody that is used in mucosal environments like the gut. It has been shown that IgA can help diversify the gut community and helps in getting rid of bacteria that cause inflammatory responses [6]. Ultimately, IgA maintains a healthy environment between the host and gut bacteria[6]. Cytokines and antibodies can also have effects outside the gut, in the lungs and other tissues.[1]
The immune system can also be altered due to the gut bacteria's ability to produce metabolites (molecules formed from metabolism) that can effect cells in the immune system. For example short chain fatty acids (SCFA) can be produced by some gut bacteria through fermentation[7]. SCFAs stimulate a rapid increase in the production of innate immune cells like neutrophils, basophils and eosinophils[7]. These cells are part of the innate immune system that try to limit the spread of infection.
--Mgsh9 (talk) 05:12, 20 November 2017 (UTC)
- ^ a b c d e f g h i j k l m n o p q r s t Sommer F, Bäckhed F (2013). "The gut microbiota—masters of host development and physiology". Nat Rev Microbiol. 11 (4): 227–38. doi:10.1038/nrmicro2974. PMID 23435359.
- ^ a b c Faderl M (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.
{{cite journal}}: Unknown parameter|displayauthors=ignored (|display-authors=suggested) (help) - ^ a b Reinoso Webb C (2016). "Protective and pro-inflammatory roles of intestinal bacteria". Pathophysiology (Review). 23 (2): 67–80. doi:10.1016/j.pathophys.2016.02.002. PMID 26947707.
- ^ a b Mantis NJ, Rol N, Corthésy B (2011). "Secretory IgA's complex roles in immunity and mucosal homeostasis in the gut". Mucosal Immunol. 4 (6): 603–11. doi:10.1038/mi.2011.41. PMC 3774538. PMID 21975936.
- ^ a b Peterson, L.W. (2014). "Intestinal epithelial cells: regulators of barrier function and immune homeostasis". Nature Reviews. Immunology. 14 (3): 141–153. doi:10.1038/nri3608. Retrieved 8 October 2017.
- ^ a b Honda, K.; Littman, D.R. (2016). "The microbiota in adaptive immune homeostasis and disease". Nature. 535: 75–84. doi:10.1038/nature18848. Retrieved 8 October 2017.
- ^ a b Levy, M.; Thaiss, C.A.; Elinav, E. (2016). "Metabolites: messengers between the microbiota and the immune system". Genes and Development. 30 (14): 1589–1597. doi:10.1101/gad.284091.116. Retrieved 8 October 2017. Cite error: The named reference "Levy" was defined multiple times with different content (see the help page).