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- W73205943 abstract "Helicobacter felis is a Gram-negative bacterium, implying the innate immune system sensing is via Toll-like receptor (TLR) 4. Yet, previous data shows TLR4 is not directly responsible for H. felis recognition. Instead, in vitro studies show TLR2 is critical in recognizing Helicobacter LPS. The project's hypothesis is if TLR2 is critical to recognition of Helicobacter, then mice engineered to be deficient in this molecule should have an altered disease process. C57BL/6 mice deficient in TLR2, TLR4, or both (TLR2/4 double knockout) were infected with H. felis and evaluated four and twelve weeks after infection. Using wildtype C57BL/6 as controls, the knockouts and controls were compared to mock infected animals of the same genotype. Surprisingly, histological inflammation in the TLR2, 4 and 2/4 knockout mice appeared similar to the infected C57BL/6 controls, indicating these recognition molecules were not critical in inflammation induction. However, IFNγ, IL-17, and TNFα mRNA levels elevated in the C57BL/6 mice post-infection were not elevated in the TLR2/4-deficient stomachs, implying in vivo recognition of Helicobacter is independent of TLR2 and 4 and other cytokines mediate this inflammation." @default.
- W73205943 created "2016-06-24" @default.
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- W73205943 date "2008-03-01" @default.
- W73205943 modified "2023-09-26" @default.
- W73205943 title "Toll‐like receptor 2 and 4 sensing in Helicobacter felis infections: implications for an alternative sensing mechanism" @default.
- W73205943 doi "https://doi.org/10.1096/fasebj.22.1_supplement.852.12" @default.
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