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(Journal of Leukocyte Biology. 2002;72:239-248.)
© 2002 by Society for Leukocyte Biology

Neutrophil-Kupffer cell interaction: a critical component of host defenses to systemic bacterial infections

Stephen H. Gregory and Edward J. Wing

Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence

Correspondence: Dr. Stephen H. Gregory, Department of Medicine, Rhode Island Hospital/Brown University School of Medicine, 432 Pierre M. Galletti Building, 55 Claverick Street, Providence, RI 02903. E-mail: sgregory{at}lifespan.org

Most bacteria that enter the bloodstream are taken up and eliminated within the liver. The specific mechanisms that underlie the role of the liver in the resolution of systemic bacterial infections remain to be determined. The vast majority of studies undertaken to date have focused on the function of resident tissue macrophages (Kupffer cells) that line the liver sinusoids. Indeed, it is often reported that Kupffer cells ingest and kill the bulk of organisms taken up by the liver. Recent studies indicate, however, that phagocytosis by Kupffer cells is not the principal mechanism by which organisms are eliminated. Rather, elimination depends on the complex interaction of Kupffer cells and bactericidal neutrophils that immigrate rapidly to the liver in response to infection. We discuss the critical role of neutrophil-Kupffer cell interaction in innate host defenses and, conceivably, the development and expression of adaptive immunity in the liver.

Key Words: septicemia • liver • macrophage • granulocyte • Listeria monocytogenes • mouse




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