Fig. 2: The molecular mechanism underlying the protective effect of H. pylori on IBD. | Cell Death & Disease

Fig. 2: The molecular mechanism underlying the protective effect of H. pylori on IBD.

From: Helicobacter pylori infection and inflammatory bowel disease: a crosstalk between upper and lower digestive tract

Fig. 2

The uncommon structure and weak biological activation of H. pylori LPS leads to the inefficient activation of NF-κB and production of low levels of proinflammatory molecules. On the other hand, H. pylori activates NOD2 and ATG16L1 to activate autophagy, and the process of autophagosome formation results in the endocytosis of MHC II and inhibition of NF-κB. The disequilibrium between inflammation and autophagy (the latter is relatively enhanced by H. pylori infection) may have a key role in the formation of tolerogenic semi-mature DCs. Moreover, NOD2 forms trimers with p38 and hnRNP-A1, and the latter subsequently enters the nucleus to stimulate IL-10 transcription. IL-10 and TGF-β are required for the activation of the Smad signaling pathway and downstream protective mechanisms, including the inhibition of TLR expression and the NK-κB signaling pathway and the induction of CDX2 production and MUC2 transcription. In addition, NLRP3 and IL-18 are indispensable for the protective effect of H. pylori on experimental colitis. Due to the NF-κB-independent production mechanism, pro-IL-18 is stably expressed in the cytoplasm and is effectively produced by activated NLRP3 and caspase-1 after H. pylori infection

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