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Lipoteichoic Acid-Induced Nitric Oxide Production Depends on the Activation of Platelet-Activating Factor Receptor and Jak2¹

Seung Hyun Han^*,, Je Hak Kim^*, Ho Seong Seo^*,, Michael H. Martin^,, Gook-Hyun Chung^*, Suzanne M. Michalek and Moon H. Nahm^2,*,

^* Department of Pathology, Department of Microbiology, and Department of Oral Biology, University of Alabama at Birmingham, Birmingham, AL 35294; and International Vaccine Institute, Seoul, Korea

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- and NO. Inhibitors of platelet-activating factor receptor (PAFR) blocked LTA- or Pam3CSK4-induced production of NO but not TNF-. Jak2 tyrosine kinase inhibition blocked LTA-induced production of NO but not TNF-. PAFR inhibition blocked phosphorylation of Jak2 and STAT1, a key factor for expressing inducible NO synthase. In addition, LTA did not induce IFN- expression, and p38 mitogen-activated protein serine kinase was necessary for LTA-induced NO production but not for TNF- 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-, 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.

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