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

Abstract

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