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The toll-like receptor 4 (TLR4) Asp299Gly polymorphism is associated with colonic localisation of Crohn’s disease without a major role for the Saccharomyces cerevisiae mannan-LBP-CD14-TLR4 pathway
  1. S Ouburg,
  2. R Mallant-Hent,
  3. J B A Crusius,
  4. A A van Bodegraven,
  5. C J J Mulder,
  6. R Linskens,
  7. A S Peña,
  8. S A Morré
  1. Laboratory of Immunogenetics and Department of Gastroenterology, VU University Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, the Netherlands
  1. Correspondence to:
    Dr S A Morré
    VU University Medical Centre, Faculty of Medicine, Laboratory of Immunogenetics, Section Immunogenetics of Infectious Diseases, Room J396, Van der Boechorststraat 7, 1081 BT Amsterdam, the Netherlands; sa.morrevumc.nl

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It is with great interest that we read the paper by Frachimont and colleagues (Gut 2004;53:987–92) in which they describe a novel association of the toll-like receptor 4 (TLR4) +896 A>G polymorphism with both Crohn’s disease (CD) and ulcerative colitis (UC), supporting the genetic influence of pattern recognition receptors (PRRs) in triggering inflammatory bowel disease (IBD). PRRs are sensors of pattern associated molecular patterns of microorganisms in the intestinal flora. Independently, we performed a similar study. However, special attention to the presence of anti-Saccharomyces cerevisiae antibody (ASCA) was taken, as Tada and colleagues1 have recently reported that the S cerevisiae mannan-LBP complex is recognised by CD14 on monocytes and signalling through TLR4 leads to the production of proinflammatory cytokines in a manner similar to that induced by lipopolysaccharide (LPS).

Patients and controls were recruited from the Outpatient Department of Gastroenterology, VU University Medical Centre, Amsterdam, the Netherlands. The group consisted of 112 CD patients and …

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  • Conflict of interest: None declared.