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Am J Physiol Lung Cell Mol Physiol 286: L1302-L1310, 2004. First published February 13, 2004; doi:10.1152/ajplung.00353.2003
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Roles for early response cytokines during Escherichia coli pneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1

Joseph P. Mizgerd,1 Michal M. Lupa,1 Josephine Hjoberg,1 Joseph C. Vallone,1 Henry B. Warren,2 James P. Butler,1 and Eric S. Silverman1

1Physiology Program, Harvard School of Public Health, and 2Center for Animal Resources and Comparative Medicine, Harvard Medical School, Boston, Massachusetts 02115

Submitted 3 October 2003 ; accepted in final form 10 February 2004

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 Escherichia 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 independently 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.

tumor necrosis factor-{alpha} receptor; interleukin-1 receptor


Address for reprint requests and other correspondence: J. P. Mizgerd, Physiology Prog., Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115 (E-mail: jmizgerd{at}hsph.harvard.edu).




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