Species-specific and pathotype-specific binding of bacteria to zymogen granule membrane glycoprotein 2 (GP2)

dc.contributor.author Schierack, Peter
dc.contributor.author Nolan, Lisa
dc.contributor.author Rödiger, Stefan
dc.contributor.author Kolenda, Rafal
dc.contributor.author Hiemann, Rico
dc.contributor.author Berger, Enrico
dc.contributor.author Grzymajło, Krzysztof
dc.contributor.author Swidsinski, Alexander
dc.contributor.author Juretzek, Thomas
dc.contributor.author Meissner, Dirk
dc.contributor.author Mydlak, Karsten
dc.contributor.author Reinhold, Dirk
dc.contributor.author Nolan, Lisa
dc.contributor.author Roggenbuck, Dirk
dc.contributor.department Veterinary Microbiology and Preventive Medicine
dc.date 2018-02-16T10:09:18.000
dc.date.accessioned 2020-07-07T05:15:15Z
dc.date.available 2020-07-07T05:15:15Z
dc.date.copyright Thu Jan 01 00:00:00 UTC 2015
dc.date.issued 2015-03-01
dc.description.abstract <p>With interest we read the paper by Juste <em>et al</em> 1 proposing the amount of zymogen-granule membrane glycoprotein 2 (GP2) on the surface of intestinal bacteria as a Crohn's disease (CD) marker. Indeed, a decreased GP2 level was found on microbes in patients with CD as compared to those of healthy controls. GP2 is a homologue to the urinary Tamm–Horsefall protein demonstrating an antimicrobial function by binding type 1-fimbriated uropathogenic <em>Escherichia coli</em> (UPEC). Likewise, GP2 seems to interact with intestinal bacteria as a specific receptor of bacterial type-1 fimbriae (FimH) on intestinal microfold cells that are partaking in immune responses against such microbes.2 GP2 is overexpressed in the inflamed intestine of patients with CD and has an immunomodulating role in innate and acquired immune responses.3 ,4Interestingly, GP2 was identified as autoantigen of pancreatic antibodies in CD.4 Altogether, these findings indicate two major GP2 sources (pancreatic/intestinal) and support a role for GP2 in the interaction between the immune system and intestinal microbiota.3 Thus, loss of tolerance to GP2 could play a role in CD's pathophysiology supposed to be exacerbated by preceding intestinal infections. In general, the findings by Juste <em>et al</em> 1 may be explained by a lower pancreatic GP2 secretion, an impaired GP2 binding to bacteria, or by a higher prevalence of bacteria with poor or no GP2 binding in patients with CD.</p>
dc.description.comments <p>This article is from <em>Gut</em> 64 (2015): 517–519, doi:<a href="http://dx.doi.org/10.1136/gutjnl-2014-307854" target="_blank">10.1136/gutjnl-2014-307854</a>. Posted with permission.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/vmpm_pubs/52/
dc.identifier.articleid 1051
dc.identifier.contextkey 7140926
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath vmpm_pubs/52
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/92358
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/vmpm_pubs/52/2015_Schierack_SpeciesSpecific.pdf|||Sat Jan 15 00:46:37 UTC 2022
dc.source.uri 10.1136/gutjnl-2014-307854
dc.subject.disciplines Veterinary Microbiology and Immunobiology
dc.title Species-specific and pathotype-specific binding of bacteria to zymogen granule membrane glycoprotein 2 (GP2)
dc.type article
dc.type.genre letter
dspace.entity.type Publication
relation.isAuthorOfPublication 9e7506b4-e945-47cf-9195-e814dac6c9fd
relation.isOrgUnitOfPublication 16f8e472-b1cd-4d8f-b016-09e96dbc4d83
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