Modulation of endotoxin-induced NF-kappa B activation in lung and liver through TNF type 1 and IL-1 receptors.
Am J Physiol Lung Cell Mol Physiol
; 283(6): L1247-54, 2002 Dec.
Article
em En
| MEDLINE
| ID: mdl-12388356
ABSTRACT
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Antígenos CD
/
NF-kappa B
/
Receptores de Interleucina-1
/
Receptores do Fator de Necrose Tumoral
/
Endotoxinas
/
Fígado
/
Pulmão
Limite:
Animals
Idioma:
En
Ano de publicação:
2002
Tipo de documento:
Article