Listeria monocytogenes-induced interferon-gamma primes the host for production of tumor necrosis factor and interferon-alpha/beta.

Abstract

Mice acquired an enhanced capacity for the production of tumor necrosis factor (TNF) and the interferons (IFN)-alpha, and -beta 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-gamma. IFN-gamma also primed infected mice for IFN-alpha/beta production. However, in addition to IFN-gamma, other L. monocytogenes-induced mechanisms endowed the host with an enhanced potential for the production of IFN-alpha/beta. Antibody-mediated depletion of various cell types in vivo revealed that CD8+ cells and NK cells are required for the production of L. monocytogenes-induced IFN-gamma during the first day of listeriosis.