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*
Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261;
Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, RI 02903; and
Department of Cell Biology, Vrije Universiteit, Amsterdam, The Netherlands
Most bacteria that enter the bloodstream are taken up by the liver.
Previously, we reported that such organisms are initially bound
extracellularly and subsequently killed by immigrating neutrophils, not
Kupffer cells as widely presumed in the literature. Rather, the
principal functions of Kupffer cells demonstrated herein are to clear
bacteria from the peripheral blood and to promote accumulation of
bactericidal neutrophils at the principal site of microbial deposition
in the liver, i.e., the Kupffer cell surface. In a mouse model of
listeriosis, uptake of bacteria by the liver at 10 min postinfection
i.v. was reduced from approximately 60% of the inoculum in normal mice
to 
15% in mice rendered Kupffer cell deficient. Immunocytochemical
analysis of liver sections derived from normal animals at 2 h
postinfection revealed the massive immigration of neutrophils and their
colocalization with Kupffer cells. Photomicrographs of the purified
nonparenchymal liver cell population derived from these infected mice
demonstrated listeriae inside neutrophils and neutrophils within
Kupffer cells. Complementary adhesion molecules promoted the
interaction between these two cell populations. Pretreatment of mice
with mAbs specific for CD11b/CD18 (type 3 complement receptor) or its
counter-receptor, CD54, inhibited the accumulation of neutrophils in
the liver and the elimination of listeriae. Complement was not a
factor; complement depletion affected neither the clearance of
listeriae by Kupffer cells nor the antimicrobial activity expressed by
infiltrating neutrophils.
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