GSE121583
NF-?B1 (p50) impairs macrophage driven inflammatory response of the host against Helicobacter pylori infection
In the present study, we observed spontaneous gastritis in 10-12 week old NF-?B1—/— mice with increased level of pro-inflammatory cytokines in gastric tissues. The NF-?B1—/— bone marrow derived macrophages showed increased level of cytokines which further exacerbated with H. pylori infection. To map the contribution of macrophages in the spontaneous gastritis, we performed comparative transcriptome analysis of NF-?B1—/— mice gastric macrophage and H. pylori treated macrophages. The transcriptome analysis showed an upregulation of innate immune response genes in NF-?B1—/— gastric macrophages, but not in H. pylori activated murine macrophages. Network analysis identified STAT1/TLR7/TLR13 as a key regulator and inhibition of STAT1 activation attenuated exacerbated innate immune response. NF-?B1—/— mice after infection with H. pylori showed increased histological gastritis and reduced level of H. pylori colonization. Our study indicates that H. pylori-mediated up-regulation of NF-?B1 mitigates host immune response and promotes chronic colonization of the pathogen. Overall design: Comparative RNA profiles of H. pylori ex-vivo activated mice gastric macrophages and  NF-?B1 knock-out/wild type mice gastric macrophages