The gene encoding for TLR9 is mapped to chromosome 3p21.3 in the vicinity http://www.selleckchem.com/products/PF-2341066.html of a shared susceptibility locus for CD and UC. Although one study has shown that the frequency of the 1237 C allele and the C carrier status were significantly increased in CD patients [14], others have shown no difference [24]. In our study, we did not observe a significant increase in this allele in our study population. There was also no association between NOD2 and TLR9 alleles in our population groups as has been shown [18]. Responses to bacterial DNA in our study were not related to the presence of particular TLR9 or NOD2 polymorphisms or to the altered expression of TLR9. Although we did not measure levels of TLR9 protein expression in these studies, it is unlikely that different levels of expression could explain our results, in that CD and UC patients did respond to bacterial DNA, but responded with a different pattern of gene expression.
It is also possible that the extensive drug usage that is characteristic of IBD patients could have affected individual host responses; however, in that the IBD patients were all on different types of medication, and the types of medication were similar between the UC and CD patients, it is unlikely that particular drug usage could be the predominant reason for the differential response between UC and CD patients. In conclusion, patients with IBD have an enhanced level of interaction between gut microbiota and the intestinal epithelium which correlates with dysregulated responses to bacterial DNA, particularly in patients with Crohn’s disease.
These results suggest that the host response to bacterial DNA may depend not only on the specific type of bacterial DNA encountered, but also on the particular host. Supporting Information Table S1 Primer Sequences. (DOC) Click here for additional data file.(28K, doc) Acknowledgments The authors would like to thank Matt Emberg for his excellent technical work in the isolating of DNA from biopsies and in carrying out the T-RFLP analysis. We would also like to thank Sue Kenney for performing the SNP analysis. Footnotes Competing Interests: The authors have declared that no competing interests exist. Funding: Canadian Institutes for Health Research, http://www.cihr-irsc.gc.ca; Crohns and Colitis Foundation of Canada, http://www.ccfc.ca; Alberta Innovates, http://www.albertainnovates.
ca; Alberta IBD Consortium, http://albertaibdconsortium.ca. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
The binder of Arl two (BART) molecule is a soluble 19-kDa protein originally purified Carfilzomib from bovine brain and identified as a binding partner of ADP-ribosylation factor-like 2 (ARL2) [1]. The binding of BART to ARL2 is of high affinity and dependent on the binding of GTP to ARL2 [1].