Nitric oxide regulates endotoxin-induced TNF-alpha production by human neutrophils.

摘要: We studied the effect of nitric oxide on LPS-induced TNF-alpha production by human neutrophils. Human neutrophils exposed to LPS and IFN-gamma did not show measurable increases in intracellular cyclic GMP (cGMP). However, cGMP increased upto 30-fold (p < 0.01) incubated with both sodium nitroprusside (SNP), an exogenous source oxide, N-acetylcysteine (NAC), which bioavailability oxide; this increase indicates that contain a oxide-sensitive guanylate cyclase. SNP, or without NAC, cultured medium alone. LPS-dependent was exposure SNP 0.05); further addition NAC 0.02). greatly LPS-mediated 0.01), plus found augment 0.01). The up-regulation associated amounts mRNA, reproduced exposing analogues. These data suggest released endothelial vascular smooth muscle cells may exert paracrine inflammatory response sepsis increasing cytokines. Although mechanism remains unknown, it does seem be dependent levels mRNA.