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Prepublished online as a Blood First Edition Paper on March 6, 2003; DOI 10.1182/blood-2002-10-3228. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: 2002-10-3228v1 102/1/328    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Henderson, R. B. Articles by Hogg, N. Search for Related Content PubMed PubMed Citation Articles by Henderson, R. B. Articles by Hogg, N. Related Collections Phagocytes Cell Adhesion and Motility Gene Expression Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 July 2003, Vol. 102, No. 1, pp. 328-335 PHAGOCYTES Rapid recruitment of inflammatory monocytes is independent of neutrophil migration Robert B. Henderson, Josie A. R. Hobbs, Meg Mathies, and Nancy Hogg From the Leukocyte Adhesion Laboratory, Cancer Research United Kingdom London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom. Early neutrophil entry into an inflammatory site is thought to mediate a chemokine switch, inducing subsequent monocyte recruitment through the regulation of monocyte chemoattractant protein-1 (MCP-1) release. As the murine monocyte is poorly characterized 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 monoclonal antibodies (mAbs) identifies 2 distinct populations, which we characterize as murine monocytes and neutrophils. Monocytes migrate in the first 2 hours of inflammation making use of 41 but not of Mac-1 or lymphocyte function-associated antigen-1 (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. 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