The action of cortisone acetate on cell-mediated immunity to infection. Suppression of host cell proliferation and alteration of cellular composition of infective foci.

Pulse labeling with tritiated thymidine shows that the response in the mouse to infection with L. monocytogenes includes a large increase in the division of lymphoid cells in the spleen, an increase in the division of macrophages in the liver, and an accumulation of monocyte-derived macrophages at infective foci in the tissues. A single 2.5 mg dose of cortisone acetate given at the beginning of infection greatly delays and suppresses these three components of the host response. The unrestricted bacterial multiplication which follows cortisone treatment is ultimately because of a failure of monocyte-derived macrophages to accumulate at infective foci where they normally express immunity. The accumulation of polymorphs at these sites, in contrast, is enhanced. It is argued that cortisone acetate prevents the accumulation of monocytes at infective foci indirectly by suppressing the production in the spleen of immunologically-committed lymphocytes which are needed to mediate the cellular events at infective foci.