scholarly journals Induction of Tumor Necrosis Factor–α Secretion and Toll‐Like Receptor 2 and 4 mRNA Expression by Genital Mucosal Fluids from Women with Bacterial Vaginosis

2005 ◽  
Vol 191 (11) ◽  
pp. 1913-1921 ◽  
Author(s):  
M. Reza Zariffard ◽  
Richard M. Novak ◽  
Nell Lurain ◽  
Beverly E. Sha ◽  
Parrie Graham ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Bacterial Vaginosis ◽  
Mrna Expression ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Vibrio vulnificus IlpA-induced Cytokine Production Is Mediated by Toll-like Receptor 2

2007 ◽  
Vol 282 (38) ◽  
pp. 27647-27658 ◽  
Author(s):  
Sung Young Goo ◽  
Yang Soo Han ◽  
Woo Hyang Kim ◽  
Kyu-Ho Lee ◽  
Soon-Jung Park
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Cytokine Production ◽  
Vibrio Vulnificus ◽  
Human Cells ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Factor Α ◽  
Necrosis Factor

Vibrio vulnificus is a pathogenic bacterium causing primary septicemia, which follows a classical septic shock pathway, including an overwhelming inflammatory cytokine response. In this study, we identified a putative lipoprotein of V. vulnificus, encoded by the ilpA gene, as one of the surface proteins that specifically reacted with the antibodies raised against outer membrane proteins of V. vulnificus. Using a mutant V. vulnificus in which its ilpA gene was knocked out, we found that IlpA is important in the production of interferon-γ in human peripheral blood mononuclear cells. Production of tumor necrosis factor-α and interleukin-6 is also induced by the recombinant IlpA (rIlpA) in human monocytes. Lipidation of the rIlpA was observed by in vivo labeling in Escherichia coli. Experiments using the mutant IlpA, which is unable to be modified by lipidation, indicate that the lipid moiety of this protein has an essential property for cytokine production in human cells. Pretreatment of monocytes with antibodies against Toll-like receptor 2 (TLR2) inhibited production of both tumor necrosis factor-α and interleukin-6. The role of TLR2 in IlpA-induced cytokine production was confirmed by an in vitro assay, in which only the TLR2-expressing cells showed a dramatic induction of nuclear factor-κB activity by rIlpA. In addition, rIlpA treatment resulted in induction of TLR2 transcription in human cells. In comparison with the wild type V. vulnificus, the ilpA mutant showed a reduced mortality in mice. These results demonstrate that IlpA of V. vulnificus functions as an immunostimulant to human cells via TLR2.

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