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1 Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and 2 Department of Pathology, University of Texas Health Science Center, Houston, Texas 77030
The initiating step of neutrophil-induced
cytotoxicity in the liver is the recruitment of these phagocytes into
sinusoids. The aim of our study was to compare the efficacy of systemic
exposure with individual inflammatory mediators on neutrophil
activation and sequestration in the hepatic vasculature of C3Heb/FeJ
mice as assessed by flow cytometry and histochemistry, respectively. The CXC chemokine macrophage inflammatory protein-2 (MIP-2; 20 µg/kg)
induced a time-dependent upregulation of Mac-1 (318% at 4 h) and
shedding of L-selectin (41% at 4 h). MIP-2 treatment caused a
temporary increase of sinusoidal neutrophil accumulation at 0.5 h
[97 ± 6 polymorphonuclear leukocytes (PMN)/50 high-power fields
(HPF)], which declined to baseline (8 ± 2) at 4 h. The CXC
chemokine KC was largely ineffective in activating neutrophils or
recruiting them into the liver. Cytokines (tumor necrosis factor-
and interleukin-1) and cobra venom factor substantially increased Mac-1 expression and L-selectin shedding on neutrophils and caused stable sinusoidal neutrophil accumulation (170-220 PMN/50 HPF). Only cytokines induced venular neutrophil margination. Thus CXC chemokines in circulation are less effective than cytokines or complement in activation of neutrophils and their recruitment into the
hepatic vasculature in vivo.
complement activation; cytokines; adhesion molecules; L-selectin; Mac-1; CD11b/CD18
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