Open AccessLipopolysaccharides from Helicobacter pylori can act as antagonists for Toll‐like receptor 4
Author(s) -
Lepper Philipp M.,
Triantafilou Martha,
Schumann Christian,
Schneider E. Marion,
Triantafilou Kathy
Publication year - 2005
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2005.00482.x
Subject(s) - tlr2 , helicobacter pylori , biology , cd14 , innate immune system , toll like receptor , tlr4 , receptor , microbiology and biotechnology , lipopolysaccharide , immune system , hek 293 cells , helicobacter , transfection , immunology , cell culture , biochemistry , genetics
Summary Infection with Helicobacter pylori , a Gram‐negative bacterium, is strongly associated with gastric ulcers and adenocarcinoma. The mechanisms by which the innate immune system recognizes H. pylori lipopolysaccharide (LPS) remain unclear. Contradictory reports exist that suggest that Toll‐like receptors are involved. In this study we evaluated the interactions of Toll‐like receptors with LPS from different strains of H. pylori . Using reporter cell lines, as well as HEK293 cells transfected with either CD14 and TLR4, or CD14 and TLR2, we show that H. pylori LPS‐induced cell activation is mediated through TLR2. In addition, for the first time, we report that LPS from some H. pylori strains are able to antagonize TLR4. The antagonistic activity of H. pylori LPS from certain strains, as well as the activation via TLR2, might give H. pylori an advantage over the host that may be associated with the clinical outcome of H. pylori infection.