alexa The heme oxygenase-1 carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1.
Pediatrics

Pediatrics

Pediatrics & Therapeutics

Author(s): Wang XM, Kim HP, Nakahira K, Ryter SW, Choi AM

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Abstract Caveolin-1 (cav-1), the principle structural protein of plasmalemmal caveolae, regulates inflammatory signaling processes originating at the membrane. We show that cav-1 bound to TLR4 and inhibited LPS-induced proinflammatory cytokine (TNF-alpha and IL-6) production in murine macrophages. Mutation analysis revealed a cav-1 binding motif in TLR4, essential for this interaction and for attenuation of proinflammatory signaling. Cav-1 was required for the anti-inflammatory effects of carbon monoxide (CO), a product of heme oxygenase-1 (HO-1) activity. CO augmented the cav-1/TLR4 interaction. Upon LPS stimulation, HO-1 trafficked to the caveolae by a p38 MAPK-dependent mechanism, where it down-regulated proinflammatory signaling. These results reveal an anti-inflammatory network involving cav-1 and HO-1. This article was published in J Immunol and referenced in Pediatrics & Therapeutics

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