Premium
Toll‐like receptor 2 and 4 sensing in Helicobacter felis infections: implications for an alternative sensing mechanism
Author(s) -
Durham Carolyn G.,
Lorenz Robin G.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.852.12
Subject(s) - tlr2 , helicobacter , tlr4 , toll like receptor , felis , innate immune system , biology , inflammation , knockout mouse , immune system , immunology , gene knockout , tlr7 , microbiology and biotechnology , pattern recognition receptor , receptor , gene , helicobacter pylori , medicine , genetics , cats
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.