A role in vivo for tumor necrosis factor alpha in host defense against Chlamydia trachomatis.
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.
Williams
D M
DM
Infectious Diseases Section, Audie L. Murphy Memorial Veterans' Hospital, San Antonio, Texas.
Magee
D M
DM
Bonewald
L F
LF
Smith
J G
JG
Bleicker
C A
CA
Byrne
G I
GI
Schachter
J
J
D000818:Animals; D002690:Chlamydia Infections / Q000503:physiopathology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008171:Lung Diseases / Q000503:physiopathology; D051379:Mice; D008819:Mice, Nude / Q000502:physiology; D011863:Radioimmunoassay; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha