Sustained Lipopolysaccharide-Induced Lung Inflammation in Mice Is Attenuated by Functional Deficiency of the Fas/Fas Ligand System-Reference-Cited by-同舟云学术

Sustained Lipopolysaccharide-Induced Lung Inflammation in Mice Is Attenuated by Functional Deficiency of the Fas/Fas Ligand System

Published:2004-03 Issue:2 Volume:11 Page:358-361
ISSN:1556-6811
Container-title:Clinical and Vaccine Immunology
language:en
Short-container-title:Clin Vaccine Immunol

Author:

Matute-Bello Gustavo¹²³⁴,Winn Robert K.¹²³⁴,Martin Thomas R.¹²³⁴,Liles W. Conrad¹²³⁴

Affiliation:

1. Medical Research Service, VA Puget Sound Health Care System

2. Divisions of Pulmonary and Critical Care Medicine

3. Allergy and Infectious Diseases, Department of Medicine

4. Department of Surgery, University of Washington School of Medicine, Seattle, Washington

Abstract

ABSTRACT To determine whether the Fas/Fas ligand (FasL) (CD95/CD178) system contributes to the development of an inflammatory response in vivo, 2.5 μg of bacterial lipopolysaccharide (LPS; endotoxin) per g was administered intranasally to healthy mice (C57BL/6) and mutant mice deficient in either Fas ( lpr mice) or FasL ( gld mice). Sustained LPS-induced neutrophilic inflammation in the lungs was attenuated in both lpr and gld mice. These observations provide further evidence of a proinflammatory role for the Fas/FasL system in the lungs.

Publisher

American Society for Microbiology

Subject

Microbiology (medical),Clinical Biochemistry,Immunology,Immunology and Allergy

Link

https://journals.asm.org/doi/pdf/10.1128/CDLI.11.2.358-361.2004

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