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

D. M. Williams, D. M. Magee, L. F. Bonewald, J. G. Smith, C. A. Bleicker, G. I. Byrne, J. Schachter

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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.

Original languageEnglish (US)
Pages (from-to)1572-1576
Number of pages5
JournalInfection and immunity
Volume58
Issue number6
StatePublished - Jan 1 1990
Externally publishedYes

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ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Cite this

Williams, D. M., Magee, D. M., Bonewald, L. F., Smith, J. G., Bleicker, C. A., Byrne, G. I., & Schachter, J. (1990). A role in vivo for tumor necrosis factor alpha in host defense against Chlamydia trachomatis. Infection and immunity, 58(6), 1572-1576.