Abstract
Mice infected iv with an immunizing dose of the gram-positive bacterium, Listeria monocytogenes, produced circulating interferon (IFN) during the inductive phase of the immune response to Listeria. Listeria infection also dramatically altered the host's responsiveness to IFN-inducing agents. Within 24 hr of infection, mice acquired a 50-fold greater than normal capacity to produce the IFNα and/or IFNβ classes (IFNα/α) following iv injection of endotoxin. Serum levels of IFNα/β peaked by 2 hr, after which high levels of IFNγ were detected in the sera of Listeria-infected mice given the B cell mitogen. Similar studies carried out with the interferon-inducing agent polyinosinic-polycytidylic acid (poly(I)·(poly(C)) revealed that mice infected for 24 hr produced only 4–8 times more IFNα/β than did noninfected mice. Unlike endotoxin, however, poly(I)·(poly(C) did not induce IFNγ in Listeria-infected animals.