Editing Helicobacter pylori (section)

===Urease===
[[File:H. pylori urease enzyme diagram.svg|thumb|''H.&nbsp;pylori'' [[urease]] enzyme diagram]]
In addition to using [[chemotaxis]] to avoid areas of high acidity (low pH), ''H.&nbsp;pylori'' also produces large amounts of [[urease]], an [[enzyme]] which breaks down the [[urea]] present in the stomach to produce [[ammonia]] and [[bicarbonate]], which are released into the bacterial cytosol and the surrounding environment, creating a neutral area.<ref name="Lin2">{{cite journal |vauthors=Lin Q, Lin S, Fan Z, Liu J, Ye D, Guo P |title=A Review of the Mechanisms of Bacterial Colonization of the Mammal Gut |journal=Microorganisms |volume=12 |issue=5 |date=May 2024 |page=1026 |pmid=38792855 |pmc=11124445 |doi=10.3390/microorganisms12051026 |doi-access=free |url=}}</ref> The decreased acidity (higher pH) changes the mucus layer from a gel-like state to a more viscous state that makes it easier for the flagella to move the bacteria through the mucosa and attach to the gastric epithelial cells.<ref name="Lin2"/> ''Helicobacter pylori'' is one of the few known types of bacterium that has a [[urea cycle]] which is uniquely configured in the bacterium.<ref name="FEMS">{{cite journal |vauthors=Hernández VM, Arteaga A, Dunn MF |title=Diversity, properties and functions of bacterial arginases |journal=FEMS Microbiol Rev |volume=45 |issue=6 |pages= |date=November 2021 |pmid=34160574 |doi=10.1093/femsre/fuab034 |url=}}</ref> 10% of the cell is of [[nitrogen]], a balance that needs to be maintained. Any excess is stored in urea excreted in the urea cycle.<ref name="FEMS" />

A final stage enzyme in the urea cycle is [[arginase]], an enzyme that is crucial to the pathogenesis of ''H. pylori''. Arginase produces [[ornithine]] and urea, which the enzyme urease breaks down into carbonic acid and ammonia. Urease is the bacterium's most abundant protein, accounting for 10–15% of the bacterium's total protein content. Its expression is not only required for establishing initial colonization in the breakdown of urea to carbonic acid and ammonia, but is also essential for maintaining chronic infection.<ref name="Li">{{cite journal |vauthors=Li S, Zhao W, Xia L, Kong L, Yang L |title=How Long Will It Take to Launch an Effective Helicobacter pylori Vaccine for Humans? |journal=Infect Drug Resist |volume=16 |issue= |pages=3787–3805 |date=2023 |pmid=37342435 |pmc=10278649 |doi=10.2147/IDR.S412361 |doi-access=free |url=}}</ref><ref name="Debowski">{{cite journal | vauthors = Debowski AW, Walton SM, Chua EG, Tay AC, Liao T, Lamichhane B, Himbeck R, Stubbs KA, Marshall BJ, Fulurija A, Benghezal M | title = Helicobacter pylori gene silencing in vivo demonstrates urease is essential for chronic infection | journal = PLOS Pathogens | volume = 13 | issue = 6 | pages = e1006464 | date = June 2017 | pmid = 28644872 | pmc = 5500380 | doi = 10.1371/journal.ppat.1006464 | doi-access = free }}</ref> Ammonia reduces stomach acidity, allowing the bacteria to become locally established. Arginase promotes the persistence of infection by consuming arginine; arginine is used by macrophages to produce nitric oxide, which has a strong antimicrobial effect.<ref name="FEMS" /><ref name="George">{{cite journal | vauthors = George G, Kombrabail M, Raninga N, Sau AK | title = Arginase of Helicobacter Gastric Pathogens Uses a Unique Set of Non-catalytic Residues for Catalysis | journal = Biophysical Journal | volume = 112 | issue = 6 | pages = 1120–1134 | date = March 2017 | pmid = 28355540 | pmc = 5376119 | doi = 10.1016/j.bpj.2017.02.009 | bibcode = 2017BpJ...112.1120G }}</ref> The ammonia produced to regulate [[pH]] is toxic to epithelial cells.<ref>{{cite journal | vauthors = Smoot DT | title = How does Helicobacter pylori cause mucosal damage? Direct mechanisms | journal = Gastroenterology | volume = 113 | issue = 6 Suppl | pages = S31-4; discussion S50 | date = December 1997 | pmid = 9394757 | doi = 10.1016/S0016-5085(97)80008-X | doi-access = free }}</ref>