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. 1990 Jun;58(6):1572–1576. doi: 10.1128/iai.58.6.1572-1576.1990

A role in vivo for tumor necrosis factor alpha in host defense against Chlamydia trachomatis.

D M Williams 1, D M Magee 1, L F Bonewald 1, J G Smith 1, C A Bleicker 1, G I Byrne 1, J Schachter 1
PMCID: PMC258678  PMID: 2341167

Abstract

In a mouse model of pneumonia caused by murine Chlamydia trachomatis (mouse pneumonitis agent [MoPn]), tumor necrosis factor alpha (TNF-alpha) antigen and bioactivity were demonstrated in vivo in the lung during MoPn infection in both athymic (nude) and heterozygous (nu/+) mice. Antibody to TNF-alpha that was exogenously given neutralized the TNF-alpha in the lung, significantly accelerated mortality, and caused a borderline increase in MoPn counts in the lung by culture in nu/+ mice. Lipopolysaccharide-induced TNF-alpha activity or injections of recombinant murine TNF-alpha significantly but modestly protected nu/+ mice against MoPn-induced mortality. TNF-alpha is produced in vivo during C. trachomatis infection and plays a role in host defense.

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Selected References

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