A role in vivo for tumor necrosis factor alpha in host defense against Chlamydia trachomatis.
AUTOR(ES)
Williams, D M
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=258678Documentos Relacionados
- A Role for Interleukin-6 in Host Defense against Murine Chlamydia trachomatis Infection
- Role of endogenous gamma interferon in host defense against Chlamydia trachomatis infections.
- Tumor necrosis factor alpha is a cytotoxin induced by murine Chlamydia trachomatis infection.
- Antibody in host defense against mouse pneumonitis agent (murine Chlamydia trachomatis).
- Bacterial evasion of host immune defense: Yersinia enterocolitica encodes a suppressor for tumor necrosis factor alpha expression.
