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Articles in PresS, published online ahead of print August 9, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00036.2002
Submitted on January 23, 2002
Accepted on July 29, 2002
B ACTIVATION IN LUNG AND LIVER THROUGH TNF TYPE 1 AND IL-1 RECEPTORS
1 Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
2 Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA; Department of Veterans Affairs Medical Center, Nashville, Tennessee, USA
3 Department of Surgery, Vanderbilt University School of Medicine, Nashville, Tennessee, USA
* To whom correspondence should be addressed. E-mail: timothy.blackwell{at}mcmail.vanderbilt.edu.
We investigated the requirement for TNF
and 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 KO) or both TNF type 1 receptor and type 1 IL-1 receptor (TNFR1/IL-1R KO).In lung tissue, NF-
B activation was similar among the groups following exposure to aerosolized LPS. After intraperitoneal (IP) injection of LPS, NF-B activation in liver was attenuated in TNFR1KO mice, and further diminished in TNFR1/IL-1R KO mice; however, in lung tissue, no impairment in NF-B activation was found in TNFR1KO mice and only a modest decrease was found in TNFR1/IL-1R KO mice. Lung concentrations of KC and MIP-2 were lower in TNFR1 KO and TNFR1/IL-1R KO mice following both aerosolized and IP 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.
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