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Species-specific and pathotype-specific binding of bacteria to zymogen granule membrane glycoprotein 2 (GP2)
  1. Peter Schierack1,
  2. Stefan Rödiger1,
  3. Rafal Kolenda1,
  4. Rico Hiemann1,
  5. Enrico Berger1,
  6. Krzysztof Grzymajło2,
  7. Alexander Swidsinski3,
  8. Thomas Juretzek4,
  9. Dirk Meissner5,
  10. Karsten Mydlak6,
  11. Dirk Reinhold7,
  12. Lisa K Nolan8,
  13. Dirk Roggenbuck1,9
  1. 1 Faculty of Natural Sciences, Brandenburg University of Technology Cottbus—Senftenberg, Senftenberg, Germany
  2. 2 University of Environmental and Life Sciences, Wroclaw, Poland
  3. 3 Innere Klinik, Gastroenterologie, Charité Humboldt Universität, Berlin, Germany
  4. 4 Carl-Thiem-Klinikum, Cottbus, Germany
  5. 5 Labor Hameln Hildesheim, Hameln, Germany
  6. 6 Gemeinschaftslabor Cottbus, Cottbus, Germany
  7. 7 Institute of Molecular and Clinical Immunology, Otto-von-Guericke University Magdeburg, Magdeburg, Germany
  8. 8 Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA
  9. 9 GA Generic Assays GmbH, Dahlewitz, Germany
  1. Correspondence to Professor Dirk Roggenbuck, Faculty of Natural Sciences, Brandenburg University of Technology Cottbus—Senftenberg, Großenhainer Str. 57, Senftenberg 01968, Germany; dirk.roggenbuck{at}hs-lausitz.de

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Dear Editor,

With interest we read the paper by Juste et al 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 Escherichia coli (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 ,4 Interestingly, 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 et al 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.

We have a longstanding interest in GP2's intestinal function and, therefore, we evaluated GP2 as receptor for intestinal bacterial pathotypes by testing the binding of 284 bacteria in a …

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