Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors.

Koay MA, Christman JW, Wudel LJ, Allos T, Cheng DS, Chapman WC, Blackwell TS
Am J Physiol Lung Cell Mol Physiol. 2002 283 (6): L1247-54

PMID: 12388356 · DOI:10.1152/ajplung.00036.2002

We investigated the requirement for tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-1 receptors in the pathogenesis of the pulmonary and hepatic responses to Escherichia coli lipopolysaccharide (LPS) by studying wild-type mice and mice deficient in TNF type 1 receptor [TNFR1 knockout (KO)] or both TNF type 1 and IL-1 receptors (TNFR1/IL-1R KO). In lung tissue, NF-kappaB activation was similar among the groups after exposure to aerosolized LPS. After intraperitoneal injection of LPS, NF-kappaB activation in liver was attenuated in TNFR1 KO mice and further diminished in TNFR1/IL-1R KO mice; however, in lung tissue, no impairment in NF-kappaB activation was found in TNFR1 KO mice and only a modest decrease was found in TNFR1/IL-1R KO mice. Lung concentrations of KC and macrophage-inflammatory peptide 2 were lower in TNFR1 KO and TNFR1/IL-1R KO mice after aerosolized and intraperitoneal LPS. We conclude that LPS-induced NF-kappaB activation in liver is mediated through TNF-alpha- and IL-1 receptor-dependent pathways, but, in the lung, LPS-induced NF-kappaB activation is largely independent of these receptors.

MeSH Terms (15)

Aerosols Animals Antigens, CD Endotoxins Injections, Intraperitoneal Lipopolysaccharides Liver Lung Mice Mice, Knockout NF-kappa B Pneumonia Receptors, Interleukin-1 Receptors, Tumor Necrosis Factor Receptors, Tumor Necrosis Factor, Type I

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