Lipoteichoic Acid-Induced Nitric Oxide Production Depends on the Activation of Platelet-Activating Factor Receptor and Jak2 | Zendy

Seung Hyun Han | Zendy; Je Hak Kim | Zendy; Ho Seong Seo | Zendy; Michael H. Martin | Zendy; GookHyun Chung | Zendy; Suzanne M. Michalek | Zendy; Moon H. Nahm | Zendy

Open Access

Lipoteichoic Acid-Induced Nitric Oxide Production Depends on the Activation of Platelet-Activating Factor Receptor and Jak2

Author(s) -

Seung Hyun Han,

Je Hak Kim,

Ho Seong Seo,

Michael H. Martin,

GookHyun Chung,

Suzanne M. Michalek,

Moon H. Nahm

Publication year - 2006

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.176.1.573

Subject(s) - lipoteichoic acid , microbiology and biotechnology , phosphorylation , signal transduction , stat1 , platelet activating factor receptor , p38 mitogen activated protein kinases , kinase , nitric oxide , tyrosine kinase , tyrosine phosphorylation , cytokine , chemistry , biochemistry , receptor , biology , protein kinase a , immunology , bacteria , endocrinology , staphylococcus aureus , antagonist , genetics

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.

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