Editing Helicobacter pylori (section)

===Cholesterol glucoside===
The outer membrane contains ''cholesterol glucoside'', a sterol glucoside that ''H. pylori'' [[Glycosylation|glycosylates]] from the [[cholesterol]] in the gastric gland cells, and inserts it into its outer membrane.<ref name="Testerman">{{cite journal | vauthors = Testerman TL, Morris J | title = Beyond the stomach: an updated view of Helicobacter pylori pathogenesis, diagnosis, and treatment | journal = World Journal of Gastroenterology | volume = 20 | issue = 36 | pages = 12781–808 | date = September 2014 | pmid = 25278678 | pmc = 4177463 | doi = 10.3748/wjg.v20.i36.12781 | type = Review | doi-access = free }}</ref> This cholesterol glucoside is important for membrane stability, morphology and immune evasion, and is rarely found in other bacteria.<ref name="Zhang">{{cite journal |vauthors=Zhang L, Xie J |title=Biosynthesis, structure and biological function of cholesterol glucoside in Helicobacter pylori: A review |journal=Medicine (Baltimore) |volume=102 |issue=36 |pages=e34911 |date=September 2023 |pmid=37682174 |pmc=10489377 |doi=10.1097/MD.0000000000034911 |url=}}</ref><ref name="Ridyard">{{cite journal |vauthors=Ridyard KE, Overhage J |title=The Potential of Human Peptide LL-37 as an Antimicrobial and Anti-Biofilm Agent |journal=Antibiotics |volume=10 |issue=6 |date=May 2021 |page=650 |pmid=34072318 |pmc=8227053 |doi=10.3390/antibiotics10060650 |doi-access=free |url=}}</ref>

The enzyme responsible for this is ''cholesteryl α-glucosyltransferase'' (αCgT or Cgt), encoded by the ''HP0421'' gene.<ref name="Hsu">{{cite journal |vauthors=Hsu CY, Yeh JY, Chen CY, Wu HY, Chiang MH, Wu CL, Lin HJ, Chiu CH, Lai CH |title=Helicobacter pylori cholesterol-α-glucosyltransferase manipulates cholesterol for bacterial adherence to gastric epithelial cells |journal=Virulence |volume=12 |issue=1 |pages=2341–2351 |date=December 2021 |pmid=34506250 |pmc=8437457 |doi=10.1080/21505594.2021.1969171 |url=}}</ref> A major effect of the depletion of host cholesterol by Cgt is to disrupt cholesterol-rich [[lipid raft]]s in the epithelial cells. Lipid rafts are involved in cell signalling and their disruption causes a reduction in the immune inflammatory response, particularly by reducing [[interferon gamma]].<ref name="Morey">{{cite journal |vauthors=Morey P, Pfannkuch L, Pang E, Boccellato F, Sigal M, Imai-Matsushima A, Dyer V, Koch M, Mollenkopf HJ, Schlaermann P, Meyer TF |title=Helicobacter pylori Depletes Cholesterol in Gastric Glands to Prevent Interferon Gamma Signaling and Escape the Inflammatory Response |journal=Gastroenterology |volume=154 |issue=5 |pages=1391–1404.e9 |date=April 2018 |pmid=29273450 |doi=10.1053/j.gastro.2017.12.008 |url=|hdl=21.11116/0000-0001-3B12-9 |hdl-access=free }}</ref> Cgt is also secreted by the type IV secretion system, and is secreted in a selective way so that gastric niches where the pathogen can thrive are created.<ref name="Hsu" /> Its lack has been shown to give vulnerability from environmental stress to bacteria, and also to disrupt CagA-mediated interactions.<ref name="Testerman" />