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Clinical and Diagnostic Laboratory Immunology, March 2004, p. 358-361, Vol. 11, No. 2
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.2.358-361.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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

Gustavo Matute-Bello,1,2* Robert K. Winn,3 Thomas R. Martin,1,2 and W. Conrad Liles4

Medical Research Service, VA Puget Sound Health Care System,1 Divisions of Pulmonary and Critical Care Medicine,2 Allergy and Infectious Diseases, Department of Medicine,4 Department of Surgery, University of Washington School of Medicine, Seattle, Washington3

Received 17 March 2003/ Returned for modification 31 October 2003/ Accepted 26 November 2003

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.

* Corresponding author. Mailing address: Pulmonary Research Group, Seattle VAMC, 1660 S. Columbian Way, 151L, Seattle, WA 98108. Phone: (206) 277-4434. Fax: (206) 768-5289. E-mail: matuteb{at}u.washington.edu.

Clinical and Diagnostic Laboratory Immunology, March 2004, p. 358-361, Vol. 11, No. 2
1071-412X/04/$08.00+0     DOI: 10.1128/CDLI.11.2.358-361.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Martin, T. R., Frevert, C. W. (2005). Innate Immunity in the Lungs. Proc Am Thorac Soc 2: 403-411 [Abstract] [Full Text]  
  • Perl, M., Chung, C.-S., Lomas-Neira, J., Rachel, T.-M., Biffl, W. L., Cioffi, W. G., Ayala, A. (2005). Silencing of Fas, but Not Caspase-8, in Lung Epithelial Cells Ameliorates Pulmonary Apoptosis, Inflammation, and Neutrophil Influx after Hemorrhagic Shock and Sepsis. Am. J. Pathol. 167: 1545-1559 [Abstract] [Full Text]  
  • Martin, T. R., Hagimoto, N., Nakamura, M., Matute-Bello, G. (2005). Apoptosis and Epithelial Injury in the Lungs. Proc Am Thorac Soc 2: 214-220 [Abstract] [Full Text]  
  • Matute-Bello, G., Lee, J. S., Liles, W. C., Frevert, C. W., Mongovin, S., Wong, V., Ballman, K., Sutlief, S., Martin, T. R. (2005). Fas-Mediated Acute Lung Injury Requires Fas Expression on Nonmyeloid Cells of the Lung. J. Immunol. 175: 4069-4075 [Abstract] [Full Text]  


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