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Am J Physiol Lung Cell Mol Physiol (February 13, 2004). doi:10.1152/ajplung.00353.2003
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Submitted on October 3, 2003
Accepted on February 10, 2004

Roles for early response cytokines during E. coli pneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1

Joseph P. Mizgerd1*, Michal M. Lupa1, Josephine Hjoberg1, Joseph C. Vallone1, Henry B. Warren2, James P. Butler1, and Eric S. Silverman1

1 Physiology Program, Harvard School of Public Health, Boston, MA, USA
2 Center for Animal Resources and Comparative Medicine, Harvard Medical School, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: jmizgerd{at}hsph.harvard.edu.

During infection, inflammation is essential for host defense, but it can injure tissues and compromise organ function. TNF-{alpha} and IL-1 ({alpha} and {beta}) are early response cytokines that facilitate inflammation. To determine the roles of these cytokines with overlapping functions, we generated mice deficient in all of the three receptors mediating their effects (TNFR1, TNFR2, and IL-1RI). During E. coli pneumonia, receptor deficiency decreased neutrophil recruitment and edema accumulation to half of the levels observed in wild type mice. Thus, these receptors contributed to maximal responses, but substantial inflammation progressed independent of them. Receptor deficiency compromised antibacterial efficacy for some infectious doses. Decreased ventilation during E. coli pneumonia was not affected by receptor deficiency. However, the loss of lung compliance during pneumonia was substantially attenuated by receptor deficiency. Thus, during E. coli pneumonia in mice, the lack of signaling from TNF-{alpha} and IL-1 decreases inflammation and preserves lung compliance.




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