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World J Gastroenterol. Aug 28, 2013; 19(32): 5238-5249
Published online Aug 28, 2013. doi: 10.3748/wjg.v19.i32.5238
Published online Aug 28, 2013. doi: 10.3748/wjg.v19.i32.5238
Figure 2 Host genetics and epigenetics alterations by commensal bacterial and self-DNA.
Alterations in intestinal microflora or host pathogen recognition functions, such as toll-like receptor (TLR)2, directly affect host DNA methylation. Endocytosis of bacterial and release of unmethylated bacterial DNA into host cell triggers inflammatory response via TLR9. Strong activation requires a purine-purine-CpG-pyrimidine-pyrimidine bacterial DNA motif. Endocytosis of CpG rich methylated self-DNA also activates TLR9 to induce similar inflammatory response via TLR9, but with on a less magnitude compared to stimulation via bacterial DNA.
- Citation: Low D, Mizoguchi A, Mizoguchi E. DNA methylation in inflammatory bowel disease and beyond. World J Gastroenterol 2013; 19(32): 5238-5249
- URL: https://www.wjgnet.com/1007-9327/full/v19/i32/5238.htm
- DOI: https://dx.doi.org/10.3748/wjg.v19.i32.5238