Journal
JOURNAL OF IMMUNOLOGY
Volume 182, Issue 6, Pages 3809-3818Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0712437
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Funding
- American Heart Association Awards [AHA 0515312U, AHA 0335035N, AHA 0525552U]
- National Institutes of Health [R01-HL60234, R01-HL55330, R01-HL079904, P01-HL70807]
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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. The Journal of Immunology, 2009, 182: 3809-3818.
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