LISTERIA-MONOCYTOGENES, BUT NOT SALMONELLA-TYPHIMURIUM, ELICITS A CD18-INDEPENDENT MECHANISM OF NEUTROPHIL EXTRAVASATION INTO THE MURINE PERITONEAL-CAVITY

This study shows that extravasation of neutrophils into the peritoneal cavities of mice in response to intraperitoneal (i.p.) inoculation of wild-type Listeria monocytogenes requires the participation of leukoc yte adhesion molecules that are different from those involved in neutr ophil recruitment in response to i.p. inoculation of Salmonella typhim urium. In the case of S. typhimurium, extensive neutrophil influx coul d be essentially abolished by treating mice with either anti-CD11b or anti-CD18 monoclonal antibodies, whereas the same monoclonal antibodie s failed to prevent neutrophil accumulation in the peritoneal cavity i n response to inoculation of L. monocytogenes. On the other hand, i.p. inoculation of a listeriolysin-negative strain of L. monocytogenes in duced a CD11b-dependent neutrophil influx. The possibility that wild-t ype L. monocytogenes, by virtue of its ability to inhabit the cytosol of the cells it infects, induces the expression of endothelial cell ad hesion molecules in the microvasculature of the peritoneal: cavity to which neutrophils adhere via leukocyte adhesion molecules distinct fro m beta-2 integrins is discussed.