Editing Urease (section)

===Action in pathogenesis===

Bacterial ureases are often the mode of [[pathogenesis]] for many medical conditions. They are associated with [[hepatic encephalopathy]] / [[Hepatic coma]], infection stones, and peptic ulceration.<ref name="mobley">{{cite journal | vauthors = Mobley HL, Hausinger RP | title = Microbial ureases: significance, regulation, and molecular characterization | journal = Microbiological Reviews | volume = 53 | issue = 1 | pages = 85–108 | date = March 1989 | doi = 10.1128/MMBR.53.1.85-108.1989 | pmid = 2651866 | pmc = 372718 }}</ref>

====Infection stones====

Infection induced urinary stones are a mixture of [[struvite]] (MgNH<sub>4</sub>PO<sub>4</sub>•6H<sub>2</sub>O) and [[carbonate]] [[apatite]] [Ca<sub>10</sub>(PO<sub>4</sub>)6•CO<sub>3</sub>].<ref name="mobley"/> These polyvalent ions are soluble but become insoluble when [[ammonia]] is produced from microbial urease during [[urea]] [[hydrolysis]], as this increases the surrounding environments [[pH]] from roughly 6.5 to 9.<ref name="mobley"/> The resultant alkalinization results in stone [[crystallization]].<ref name="mobley"/> In humans the microbial urease, ''Proteus mirabilis'', is the most common in infection induced urinary stones.<ref name="pmid3524996">{{cite journal | vauthors = Rosenstein IJ | title = Urinary Calculi: Microbiological and Crystallographic Studies | journal = Critical Reviews in Clinical Laboratory Sciences | volume = 23 | issue = 3 | pages = 245–277 | date = 1 January 1986 | pmid = 3524996 | doi = 10.3109/10408368609165802 }}</ref>

====Urease in hepatic encephalopathy / hepatic coma====

Studies have shown that ''[[Helicobacter pylori]]'' along with [[cirrhosis]] of the liver cause [[hepatic encephalopathy]] and [[hepatic coma]].<ref name="agrawal">{{cite journal | vauthors = Agrawal A, Gupta A, Chandra M, Koowar S | title = Role of Helicobacter pylori infection in the pathogenesis of minimal hepatic encephalopathy and effect of its eradication | journal = Indian Journal of Gastroenterology | volume = 30 | issue = 1 | pages = 29–32 | date = 17 March 2011 | pmid = 21416318 | doi = 10.1007/s12664-011-0087-7 | s2cid = 25452909 }}</ref> ''Helicobacter pylori''  release microbial ureases into the stomach. The urease hydrolyzes [[urea]] to produce [[ammonia]] and [[carbonic acid]]. As the bacteria are localized to the stomach [[ammonia]] produced is readily taken up by the [[circulatory system]] from the gastric [[lumen (anatomy)|lumen]].<ref name="agrawal"/> This results in elevated [[ammonia]] levels in the blood, a condition known as [[hyperammonemia]]; eradication of ''Helicobacter pylori'' show marked decreases in [[ammonia]] levels.<ref name="agrawal"/>

====Urease in peptic ulcers====

''Helicobacter pylori'' is also the cause of peptic ulcers with its manifestation in 55–68% reported cases.<ref name="tang">{{cite journal | vauthors = Tang JH, Liu NJ, Cheng HT, Lee CS, Chu YY, Sung KF, Lin CH, Tsou YK, Lien JM, Cheng CL | title = Endoscopic diagnosis of Helicobacter pylori infection by rapid urease test in bleeding peptic ulcers: a prospective case-control study | journal = Journal of Clinical Gastroenterology | volume = 43 | issue = 2 | pages = 133–9 | date = February 2009 | pmid = 19230239 | doi = 10.1097/MCG.0b013e31816466ec | s2cid = 27784917 }}</ref>  This was confirmed by decreased [[ulcer]] bleeding and [[ulcer]] reoccurrence after eradication of the [[pathogen]].<ref name="tang"/> In the stomach there is an increase in [[pH]] of the mucosal lining as a result of [[urea]] [[hydrolysis]], which prevents movement of [[hydrogen ions]] between gastric glands and gastric [[lumen (anatomy)|lumen]].<ref name="mobley"/>  In addition, the high [[ammonia]] concentrations have an effect on intercellular [[tight junctions]] increasing permeability and also disrupting the gastric [[mucous membrane]] of the stomach.<ref name="mobley"/><ref>{{cite journal | vauthors = Caron TJ, Scott KE, Fox JG, Hagen SJ | title = Tight junction disruption: Helicobacter pylori and dysregulation of the gastric mucosal barrier | journal = World Journal of Gastroenterology | volume = 21 | issue = 40 | pages = 11411–27 | date = October 2015 | pmid = 26523106 | pmc = 4616217 | doi = 10.3748/wjg.v21.i40.11411 | doi-access = free }}</ref>