Listeria monocytogenes-Induced Interferon-v Primes the Host for Production of Tumor Necrosis Factor and Interferon-α/β

Mice acquired an enhanced capacity for the production of tumor necrosis factor (TNF) and the interferons (IFN)-α, and -β shortly after intravenous injection of viable Listeria monocytogenes. By the end of the first day of a sublethal infection, mice were primed to produce 100-1000 times more endotoxin-induced serum TNF than is produced by normal mice. Acquisition of the augmented capacity for TNF production was due to L. monocytogenes-induced IFN-γ. IFN-γ also primed infected mice for IFN-α/β production. However, in addition to IFN-γ, other L. monocytogenes-induced mechanisms endowed the host with an enhanced potential for the production of IFN-α/β