| First Author | Wang XM | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 6 | Pages | 3809-18 |
| PubMed ID | 19265160 | Mgi Jnum | J:145914 |
| Mgi Id | MGI:3836322 | Doi | 10.4049/jimmunol.0712437 |
| Citation | Wang XM, et al. (2009) The heme oxygenase-1/carbon monoxide pathway suppresses TLR4 signaling by regulating the interaction of TLR4 with caveolin-1. J Immunol 182(6):3809-18 |
| abstractText | 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. |
