Editing Gastrointestinal tract (section)

====Immune function====
The gastrointestinal tract forms an important part of the [[immune system]].<ref>{{Cite journal|last1=Mowat|first1=Allan M.|last2=Agace|first2=William W.|date=2014-10-01|title=Regional specialization within the intestinal immune system|journal=Nature Reviews. Immunology|volume=14|issue=10|pages=667–685|doi=10.1038/nri3738|issn=1474-1741|pmid=25234148|s2cid=31460146}}</ref>

=====Immune barrier=====
The surface area of the digestive tract is estimated to be about 32 square meters, or about half a badminton court.<ref name="ReferenceA" /> With such a large exposure (more than three times larger than the [[Human skin|exposed surface of the skin]]), these immune components function to prevent pathogens from entering the blood and lymph circulatory systems.<ref>{{Cite journal|last1= Flannigan|first1=Kyle L.|last2=Geem|first2=Duke|last3=Harusato|first3=Akihito|last4=Denning|first4=Timothy L.|date=2015-07-01|title=Intestinal Antigen-Presenting Cells: Key Regulators of Immune Homeostasis and Inflammation|journal=The American Journal of Pathology|volume=185|issue=7|pages=1809–1819|doi= 10.1016/j.ajpath.2015.02.024|issn=1525-2191|pmc=4483458|pmid=25976247}}</ref> Fundamental components of this protection are provided by the [[intestinal mucosal barrier]], which is composed of physical, biochemical, and immune elements elaborated by the intestinal mucosa.<ref>{{Cite journal|last1=Sánchez de Medina|first1=Fermín|last2=Romero-Calvo|first2=Isabel|last3=Mascaraque|first3=Cristina|last4=Martínez-Augustin|first4=Olga|date=2014-12-01|title= Intestinal inflammation and mucosal barrier function|journal=Inflammatory Bowel Diseases|volume=20|issue=12|pages= 2394–2404|doi=10.1097/MIB.0000000000000204|issn=1536-4844|pmid=25222662|s2cid=11434730|doi-access=free}}</ref> Microorganisms also are kept at bay by an extensive immune system comprising the [[gut-associated lymphoid tissue]] (GALT).

There are additional factors contributing to protection from pathogen invasion. For example, low [[pH]] (ranging from 1 to 4) of the stomach is fatal for many [[microorganism]]s that enter it.<ref>{{Cite journal|last=Schubert|first=Mitchell L.|date=2014-11-01|title=Gastric secretion|journal=Current Opinion in Gastroenterology|volume=30|issue=6|pages=578–582|doi=10.1097/MOG.0000000000000125|issn=1531-7056|pmid=25211241|s2cid=8267813}}</ref> Similarly, [[mucus]] (containing [[IgA]] [[antibody|antibodies]]) neutralizes many pathogenic microorganisms.<ref>{{Cite journal|last1=Márquez|first1=Mercedes|last2=Fernández Gutiérrez Del Álamo|first2=Clotilde|last3=Girón-González|first3=José Antonio|date=2016-01-28|title=Gut epithelial barrier dysfunction in human immunodeficiency virus-hepatitis C virus coinfected patients: Influence on innate and acquired immunity|journal=World Journal of Gastroenterology|volume=22|issue=4|pages=1433–1448|doi=10.3748/wjg.v22.i4.1433|issn=2219-2840|pmc=4721978|pmid=26819512|doi-access=free}}</ref> Other factors in the GI tract contribution to immune function include [[enzyme]]s secreted in the [[saliva]] and [[bile]].

=====Immune system homeostasis=====
Beneficial bacteria also can contribute to the homeostasis of the gastrointestinal immune system. For example, [[Clostridia]], one of the most predominant bacterial groups in the GI tract, play an important role in influencing the dynamics of the gut's immune system.<ref>{{Cite journal|title=Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells|journal=Nature|volume=504|issue=7480|pages=446–450|doi=10.1038/nature12721|pmid=24226770|year=2013|last1=Furusawa|first1=Yukihiro|last2=Obata|first2=Yuuki|last3=Fukuda|first3=Shinji|last4=Endo|first4=Takaho A.|last5=Nakato|first5=Gaku|last6=Takahashi|first6=Daisuke|last7=Nakanishi|first7=Yumiko|last8=Uetake|first8=Chikako|last9=Kato|first9=Keiko|last10=Kato|first10=Tamotsu|last11=Takahashi|first11=Masumi|last12=Fukuda|first12=Noriko N.|last13=Murakami|first13=Shinnosuke|last14=Miyauchi|first14=Eiji|last15=Hino|first15=Shingo|last16=Atarashi|first16=Koji|last17=Onawa|first17=Satoshi|last18=Fujimura|first18=Yumiko|last19=Lockett|first19=Trevor|last20=Clarke|first20=Julie M.|last21=Topping|first21=David L.|last22=Tomita|first22=Masaru|last23=Hori|first23=Shohei|last24=Ohara|first24=Osamu|last25=Morita|first25=Tatsuya|last26=Koseki|first26=Haruhiko|last27=Kikuchi|first27=Jun|last28=Honda|first28=Kenya|last29=Hase|first29=Koji|last30=Ohno|first30=Hiroshi|bibcode=2013Natur.504..446F|s2cid=4408815}}</ref> It has been demonstrated that the intake of a high fiber diet could be responsible for the induction of [[T-regulatory cell]]s (Tregs). This is due to the production of [[short-chain fatty acid]]s during the fermentation of plant-derived nutrients such as [[butyrate]] and [[propionate]]. Basically, the butyrate induces the differentiation of Treg cells by enhancing [[histone H3]] [[Acetylation#Protein acetylation|acetylation]] in the promoter and conserved non-coding sequence regions of the [[FOXP3]] locus, thus regulating the [[T cells]], resulting in the reduction of the inflammatory response and allergies.