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*
Department of Pathology and
Graduate Program in Cellular and Molecular Biology, University of Michigan Medical Center, and
Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI 48109
Neutrophils (polymorphonuclear leukocytes; PMN) are phagocytic
cells instrumental in the clearance of infectious pathogens. Human PMN
are commonly thought to respond primarily to chemokines from the CXC
family. However, recent findings suggest that under specific cytokine
activation conditions, PMN can also respond to some CC chemokines. In
this study, the effect of GM-CSF, a well-characterized PMN priming and
maturation factor, on CC-chemokine receptor (CCR) expression in PMN was
investigated. Constitutive expression of CCR1 and CCR3 mRNA in PMN was
detected by ribonuclease protection assay. Following incubation of PMN
with GM-CSF (0.01–10 ng/ml; 6 h) CCR1 mRNA expression was rapidly
(
1 h) up-regulated. In contrast, no significant induction of CCR2,
CCR3, CCR4, or CCR5 mRNA was observed. CCR1 protein was also
up-regulated by GM-CSF stimulation. GM-CSF-induced up-regulation of
CCR1 showed functional consequences because GM-CSF-treated PMN, but not
control cells, responded to the CC chemokines macrophage inflammatory
protein-1
, monocyte chemoattractant protein-3, and RANTES in assays
of chemotactic migration and intracellular calcium mobilization. These
results suggest that PMN activated by the proinflammatory cytokine
GM-CSF can change their receptor expression pattern and become
responsive to CC chemokines.
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