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 leukocyte adhesion molecules that are different from those involved in neutrophil recruitment in response to i.p. inoculation of Salmonella typhimurium. In the case of S. typhimurium, extensive neutrophil influx could be essentially abolished by treating mice with either anti-CD11b or anti-CD18 monoclonal antibodies, whereas the same monoclonal antibodies failed to prevent neutrophil accumulation in the peritoneal cavity in response to inoculation of L. monocytogenes. On the other hand, i.p. inoculation of a listeriolysin-negative strain of L. monocytogenes induced a CD11b-dependent neutrophil influx. The possibility that wild-type L. monocytogenes, by virtue of its ability to inhabit the cytosol of the cells it infects, induces the expression of endothelial cell adhesion molecules in the microvasculature of the peritoneal cavity to which neutrophils adhere via leukocyte adhesion molecules distinct from beta-2 integrins is discussed.