Open AccessToll‐like receptors 1 and 2 cooperatively mediate immune responses to curli, a common amyloid from enterobacterial biofilms
Author(s) -
Tükel Çagla,
Nishimori Jessalyn H.,
Wilson R. Paul,
Winter Maria G.,
Keestra A. Marijke,
Van Putten Jos P. M.,
Bäumler Andreas J.
Publication year - 2010
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.1462-5822.2010.01485.x
Subject(s) - tlr2 , biofilm , biology , microbiology and biotechnology , salmonella enterica , immune system , toll like receptor , receptor , innate immune system , bacteria , salmonella , immunology , biochemistry , genetics
Summary Responses to host amyloids and curli amyloid fibrils of Escherichia coli and Salmonella enterica serotype Typhimurium are mediated through Toll‐like receptor (TLR) 2. Here we show that TLR2 alone was not sufficient for mediating responses to curli. Instead, transfection experiments with human cervical cancer (HeLa) cells and antibody‐mediated inhibition of TLR signalling in human macrophage‐like (THP‐1) cells suggested that TLR2 interacts with TLR1 to recognize curli amyloid fibrils. TLR1/TLR2 also serves as a receptor for tri‐acylated lipoproteins, which are produced by E. coli and other Gram‐negative bacteria. Despite the presence of multiple TLR1/TLR2 ligands on intact bacterial cells, an inability to produce curli amyloid fibrils markedly reduced the ability of E. coli to induce TLR2‐dependent responses in vitro and in vivo . Collectively, our data suggest that curli amyloid fibrils from enterobacterial biofilms significantly contribute to TLR1/TLR2‐mediated host responses against intact bacterial cells.