Mechanism of resistance to Listeria monocytogenes in splenectomized mice

Abstract

The present study is an investigation of the basis of the enhanced antilisterial resistance exhibited by splenectomized mice. The response of the mononuclear phagocyte system of these hosts has been extensively investigated as a result of the finding that enhanced antilisterial resistance in these hosts is abolished by treatment with silica. Splenectomized mice demonstrate a quantitatively greater influx of immature macrophage precursors in response to listerial infection and intraperitoneal stimuli. Despite the higher responsiveness of immature macrophage precursors in the splenectomized host, radiation studies have determined that antilisterial resistance in splenectomized mice is provided by the mature mononuclear phagocytes of the liver, the Kupffer cells. However, Kupffer cells of splenectomized mice exhibit the same level of function associated with listericidal activity as non-splenectomized animals. An examination of the cellular composition of the spleen at early time intervals following infection with Listeria has led to the conclusion that enhanced antilisterial resistance in splenectomized mice may be explained on the basis of the loss of a storage function of the spleen. In the absence of the spleen, leucocytes are made available for migration to the liver upon infection of the host. The early destruction of Listeria which presumably results, is responsible for the lower growth of the organism measured at 48 hours post-infection