Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 7, Pages 4641-4646Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.7.4641
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The pathogenesis of Mycoplasma pneumoniae infection is considered to be in part attributed to excessive immune responses. Recently, lipoproteins from mycoplasmas have been reported to induce NF-kappa B activation. In this study, we examined the ability of lipoproteins from M. pneumoniae to activate NF-kappa B, and the active component responsible for the NF-kappa B activation was identified. Lipid-associated membrane proteins from M. pneumoniae were found to induce NF-kappa B through TLR 2 in a human monocytic cell line, THP-1. The active component of the Lipid-associated membrane proteins was a subunit b of F0F1-type ATPase (F0F1-ATPase). The F0F1-ATPase is assumed to contain two palmitic acids. The activation of NF-kappa B by the F0F1-ATPase was inhibited by a dominant negative construct of TLR1 and TLR6. These results indicate that the activation of NF-kappa B by F(0)F(1-)ATPase is dependent on TLR1, TLR2, and TLR6. The activity of the F0F1-ATPase was decreased with pretreatment of lipoprotein lipase but not protease, indicating that the lipid moiety of the F0F1-ATPase was important for the NF-kappa B activation. Thus, a dipalmitoylated lipoprotein from M. pneumoniae was found to activate NF-kappa B through TLR1, TLR2, and TLR6.
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