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Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2002-10-3228.

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Submitted October 24, 2002
Accepted February 19, 2003

Rapid recruitment of inflammatory monocytes is independent of neutrophil migration

Robert B Henderson, Josie A R Hobbs, Meg Mathies, and Nancy Hogg*

Leukocyte Adhesion Laboratory, Cancer Research UK London Research Institute, London, United Kingdom

* Corresponding author; email: nancy.hogg{at}cancer.org.uk.

Early neutrophil entry into an inflammatory site is thought to mediate a chemokine switch, inducing subsequent monocyte recruitment through the regulation of MCP-1 release. As the murine monocyte is poorly characterised and difficult to identify, there has been little examination of either its early recruitment in inflammatory models or of the factors that influence its early migration. The phenotyping of rapidly recruited inflammatory leukocytes with 7/4 and Gr-1 mAbs identifies two distinct populations, which we characterise as murine monocytes and neutrophils. Monocytes migrate in the first two hours of inflammation making use of {alpha}4{beta}1, but not Mac-1 or LFA-1 integrins. Early migration is dependent on MCP-1, but neither MCP-1 release, nor monocyte recruitment is affected by the reduced neutrophil migration seen in LFA-1-/- mice. Endogenous peritoneal macrophages and mesothelial cells lining the peritoneum contain MCP-1, which is released following thioglycollate stimulation. The murine monocyte therefore responds rapidly to chemokines produced in situ by tissue cells at the site of inflammation with no requirement for prior influx of neutrophils.


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