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The present study was conducted to determine the extent to which the cytokines tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) are required to protect against primary or secondary murine tularaemia caused by the live vaccine strain of the facultative intracellular bacterium  Francisella tularensis . It is shown that non-immune mice treated with neutralizing monoclonal antibodies (mAbs) against TNF-α and IFN-γ are rendered defenceless against otherwise sublethal intravenous inocula of the bacterium. Treatment with either of the anti-cytokine mAbs resulted in even a very small inoculum of 500 c.f.u. of the pathogen multiplying unrestrictedly in the livers, spleens and lungs of non-immune mice to rapidly reach lethal numbers. By contrast,  Francisella -immune mice treated with either of the mAbs remained capable of resolving secondary infection with 50-fold larger inocula. However, the need for TNF-α and IFN-γ for controlling secondary tularaemia became critical when challenge inocula exceeded 10 6  c.f.u. Overall, the results imply that different defence mechanisms operate to control primary versus secondary murine tularaemia. Additionally, they show that the need for TNF-α and IFN-γ to combat secondary infection depends on the size of the challenge inoculum.

microbiology

The requirement of tumour necrosis factor-α and interferon-γ for the expression of protective immunity to secondary murine tularaemia depends on the size of the challenge inoculum