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GRO family chemokines are specialized for monocyte arrest from flow

¹Department of Molecular Physiology, ²Cardiovascular Research Center, and ³Department of Biomedical Engineering, University of Virginia, Charlottesville, Virginia

Submitted 15 February 2005 ; accepted in final form 1 June 2005

Chemokines participate in various processes of monocyte recruitment including monocyte arrest and migration. Our group and others have demonstrated that growth-related oncogene (GRO)- (CXCL1) can support monocyte arrest in models of inflammation. Here we employed a parallel plate-flow chamber and Transwell reconstitution assay to test whether GRO family chemokines were sufficient for Mono Mac 6 (a human monocytic cell line) and isolated human monocyte recruitment. Our study shows that 1) GRO-, - (CXCL2), and - (CXCL3) all act as arrest chemokines for monocyte adhesion on vascular cell adhesion molecule (VCAM)-1 under flow in the presence of P-selectin; 2) CXCR2 is the functional receptor for GRO-family chemokines in monocyte arrest; however, CXCR2 is not an arrest chemokine receptor in general, since epithelial neutrophil-activating peptide ENA-78 failed to arrest monocytes; 3) GRO-, -, and - all fail to increase intracellular free Ca²⁺ or mediate monocyte chemotaxis; and 4) signaling through G_i protein, phosphoinositide 3-kinase, and actin polymerization but not Ca²⁺ mobilization or the mitogen-activated kinases p38 and MAPK/extracellular signal-related kinase are necessary for GRO--mediated Mono Mac 6 cell arrest under flow. We conclude that the GRO-family chemokines are specialized monocyte-arrest chemokines. Their role in monocyte recruitment in inflammation can be inhibited by blocking CXCR2 function or downstream signaling events.

growth-related oncogene; P-selectin; vascular cell adhesion molecule-1; phosphoinositide 3-kinase; G protein; signaling

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