Abstract
G A A b st ra ct s colonization was significantly lower compared with wild-type controls, whereas inflammatory cells infiltration in gastric mucosa and pro-inflammatory cytokines/chemokines production were significantly increased compared with infected controls. Intriguingly, in MyD88 and OLFM4 double knockout mice, the H. pylori colonization, inflammatory cells infiltration in the gastric mucosa and proinflammatory cytokines/chemokines expression were all attenuated to a similar extent as wild-type controls. In addition to these phenomena, we also observed that, although it did not bind directly with MyD88, OLFM4 could bind with nucleotide oligomerization domain-2 (NOD2). OLFM4 deletion enhanced NOD2 expression, and thereby further increased MyD88 expression. Together, our results suggest that MyD88 is a downstream mediator involved in the regulatory network of OLFM4 on host immunity against H. pylori infection.
Published Version
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