Role of tumor necrosis factor alpha in pathogenesis of pneumococcal pneumonia in mice

Abstract

The production and role of tumor necrosis factor alpha (TNF-α) in pneumococcal pneumonia were investigated in a mouse pneumonia model. When approximately 106 CFU of Streptococcus pneumoniae TUM19 were used to inoculate CBA/J mice intranasally, TNF-α levels in the lungs and serum began to increase from 1 and 3 days after infection, respectively, concomitantly with the increase in bacterial counts in the lungs. Anti-TNF-α antibody accelerated bacterial proliferation in the blood and the death of the mice. Although serum levels of immunoglobulin G antibody against the infecting bacteria were not affected by the anti-TNF-α antibody treatment, neutrophil counts in the blood were decreased by the treatment. These results suggest that TNF-α produced in the course of pneumococcal pneumonia prevents bacteremia by increasing the number of neutrophils in the blood.