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

Departments of 1  Medicine and 2  Surgery, Vanderbilt University School of Medicine, Nashville 37232-2650; and 3  Department of Veterans Affairs Medical Center, Nashville, Tennessee 37203 We investigated the requirement for tumor necrosis factor- (TNF- ) and interleukin (IL)-1 receptors in the patho...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Lung cellular and molecular physiology 2002-12, Vol.283 (6), p.1247-L1254
Main Authors: Koay, M. Audrey, Christman, John W, Wudel, L. James, Allos, Tara, Cheng, Dong-Sheng, Chapman, William C, Blackwell, Timothy S
Format: Article
Language:English
Subjects:
Aerosols
Animals
Antigens, CD - physiology
Endotoxins - pharmacology
Injections, Intraperitoneal
Lipopolysaccharides - administration & dosage
Liver - metabolism
Lung - metabolism
Mice
Mice, Knockout - genetics
NF-kappa B - physiology
Pneumonia - chemically induced
Receptors, Interleukin-1 - physiology
Receptors, Tumor Necrosis Factor - physiology
Receptors, Tumor Necrosis Factor, Type I
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Departments of 1  Medicine and 2  Surgery, Vanderbilt University School of Medicine, Nashville 37232-2650; and 3  Department of Veterans Affairs Medical Center, Nashville, Tennessee 37203 We investigated the requirement for tumor necrosis factor- (TNF- ) 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- B activation was similar among the groups after exposure to aerosolized LPS. After intraperitoneal injection of LPS, NF- B 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- B 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- B activation in liver is mediated through TNF- - and IL-1 receptor-dependent pathways, but, in the lung, LPS-induced NF- B activation is largely independent of these receptors. sepsis; macrophage; neutrophil; cytokines; chemokines
ISSN:1040-0605
1522-1504
DOI:10.1152/ajplung.00036.2002