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 IFN alpha and/or IFN beta classes (IFN alpha/beta) following iv injection of endotoxin. Serum levels of IFN alpha/beta peaked by 2 hr, after which high levels of IFN gamma 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 IFN alpha/beta than did noninfected mice. Unlike endotoxin, however, poly(I).poly(C) did not induce IFN gamma in Listeria-infected animals.
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