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Helicobacter pylori
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===Adhesins=== ''H. pylori'' must make attachment with the epithelial cells to prevent its being swept away with the constant movement and renewal of the mucus. To give them this adhesion, [[Bacterial outer membrane#Outer membrane proteins|bacterial outer membrane proteins]] as virulence factors called [[bacterial adhesin|adhesins]] are produced.<ref name="Doohan">{{cite journal |vauthors=Doohan D, Rezkitha YA, Waskito LA, Yamaoka Y, Miftahussurur M |title=Helicobacter pylori BabA-SabA Key Roles in the Adherence Phase: The Synergic Mechanism for Successful Colonization and Disease Development |journal=Toxins |volume=13 |issue=7 |date=July 2021 |page=485 |pmid=34357957 |pmc=8310295 |doi=10.3390/toxins13070485 |doi-access=free |url=}}</ref> BabA (blood group antigen binding adhesin) is most important during initial colonization, and SabA (sialic acid binding adhesin) is important in persistence. BabA attaches to glycans and mucins in the epithelium.<ref name="Doohan"/> BabA (coded for by the ''babA2'' gene) also binds to the [[Lewis antigen system|Lewis b antigen]] displayed on the surface of the epithelial cells.<ref name="Rad">{{cite journal |last1=Rad |first1=Roland |last2=Gerhard |first2=Markus |last3=Lang |first3=Roland |last4=Schöniger |first4=Martin |last5=Rösch |first5=Thomas |last6=Schepp |first6=Wolfgang |last7=Becker |first7=Ingrid |last8=Wagner |first8=Hermann |last9=Prinz |first9=Christian |title=The Helicobacter pylori Blood Group Antigen-Binding Adhesin Facilitates Bacterial Colonization and Augments a Nonspecific Immune Response |journal=The Journal of Immunology |date=15 March 2002 |volume=168 |issue=6 |pages=3033–3041 |doi=10.4049/jimmunol.168.6.3033|pmid=11884476 |doi-access=free }}</ref> Adherence via BabA is acid sensitive and can be fully reversed by a decreased pH. It has been proposed that BabA's acid responsiveness enables adherence while also allowing an effective escape from an unfavorable environment such as a low pH that is harmful to the organism.<ref>{{cite journal | vauthors = Bugaytsova JA, Björnham O, Chernov YA, Gideonsson P, Henriksson S, Mendez M, Sjöström R, Mahdavi J, Shevtsova A, Ilver D, Moonens K, Quintana-Hayashi MP, Moskalenko R, Aisenbrey C, Bylund G, Schmidt A, Åberg A, Brännström K, Königer V, Vikström S, Rakhimova L, Hofer A, Ögren J, Liu H, Goldman MD, Whitmire JM, Ådén J, Younson J, Kelly CG, Gilman RH, Chowdhury A, Mukhopadhyay AK, Nair GB, Papadakos KS, Martinez-Gonzalez B, Sgouras DN, Engstrand L, Unemo M, Danielsson D, Suerbaum S, Oscarson S, Morozova-Roche LA, Olofsson A, Gröbner G, Holgersson J, Esberg A, Strömberg N, Landström M, Eldridge AM, Chromy BA, Hansen LM, Solnick JV, Lindén SK, Haas R, Dubois A, Merrell DS, Schedin S, Remaut H, Arnqvist A, Berg DE, Borén T | title = Helicobacter pylori Adapts to Chronic Infection and Gastric Disease via pH-Responsive BabA-Mediated Adherence | journal = Cell Host & Microbe | volume = 21 | issue = 3 | pages = 376–389 | date = March 2017 | pmid = 28279347 | pmc = 5392239 | doi = 10.1016/j.chom.2017.02.013 }}</ref> SabA (coded for by the ''sabA'' gene) binds to increased levels of [[sialyl-Lewis x|sialyl-Lewis <sup>X</sup>]] antigen expressed on gastric mucosa.<ref name="pmid12142529">{{cite journal | vauthors = Mahdavi J, Sondén B, Hurtig M, Olfat FO, Forsberg L, Roche N, Angstrom J, Larsson T, Teneberg S, Karlsson KA, Altraja S, Wadström T, Kersulyte D, Berg DE, Dubois A, Petersson C, Magnusson KE, Norberg T, Lindh F, Lundskog BB, Arnqvist A, Hammarström L, Borén T | title = Helicobacter pylori SabA adhesin in persistent infection and chronic inflammation | journal = Science | volume = 297 | issue = 5581 | pages = 573–8 | date = July 2002 | pmid = 12142529 | pmc = 2570540 | doi = 10.1126/science.1069076 | bibcode = 2002Sci...297..573M }}</ref>
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