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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Lipoteichoic acid-induced nitric oxide production depends on the activation of platelet-activating factor receptor and Jak2.

NO production by macrophages in response to lipoteichoic acid (LTA) and a synthetic lipopeptide (Pam3CSK4) was investigated. LTA and Pam3CSK4 induced the production of both TNF-alpha and NO. Inhibitors of platelet-activating factor receptor (PAFR) blocked LTA- or Pam3CSK4- induced production of NO but not TNF-alpha. Jak2 tyrosine kinase inhibition blocked LTA- induced production of NO but not TNF-alpha. PAFR inhibition blocked phosphorylation of Jak2 and STAT1, a key factor for expressing inducible NO synthase. In addition, LTA did not induce IFN-beta expression, and p38 mitogen- activated protein serine kinase was necessary for LTA- induced NO production but not for TNF-alpha production. These findings suggest that Gram-positive bacteria induce NO production using a PAFR signaling pathway to activate STAT1 via Jak2. This PAFR/Jak2/STAT1 signaling pathway resembles the IFN-beta, type I IFNR/Jak/STAT1 pathway described for LPS. Consequently, Gram-positive and Gram-negative bacteria appear to have different but analogous mechanisms for NO production.[1]

References

  1. Lipoteichoic acid-induced nitric oxide production depends on the activation of platelet-activating factor receptor and Jak2. Han, S.H., Kim, J.H., Seo, H.S., Martin, M.H., Chung, G.H., Michalek, S.M., Nahm, M.H. J. Immunol. (2006) [Pubmed]
 
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