The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/9/741/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 5, September 6, 1999 741-748

Brief Definitive Report

N-Formylpeptides Induce Two Distinct Concentration Optima for Mouse Neutrophil Chemotaxis by Differential Interaction with Two N-Formylpeptide Receptor (Fpr) Subtypes: Molecular Characterization of Fpr2, a Second Mouse Neutrophil Fpr



Jennifer K. Hartta, Grant Barisha, Philip M. Murphya, and Ji-Liang Gaoa

a From the Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892
Laboratory of Host Defenses, NIAID, Bldg. 10, Rm. 11N113, National Institutes of Health, Bethesda, MD 20892.301-402-4369301-496-2877

jgao{at}nih.gov

The N-formylpeptide receptor (FPR) is a G protein–coupled receptor that mediates mammalian phagocyte chemotactic responses to bacterial N-formylpeptides. Here we show that a mouse gene named Fpr-rs2 encodes a second N-formylpeptide receptor subtype selective for neutrophils which we have provisionally named FPR2. The prototype N-formylpeptide fMLF induced calcium flux and chemotaxis in human embryonic kidney (HEK) 293 cells stably transfected with FPR2. The EC50s, ~5 µM for calcium flux and chemotaxis, were ~100-fold greater than the corresponding values for mouse FPR-transfected HEK 293 cells. Consistent with this, fMLF induced two distinct concentration optima for chemotaxis of normal mouse neutrophils, but only the high concentration optimum for chemotaxis of neutrophils from FPR knockout mice. Based on these data, we hypothesize that high- and low-affinity N-formylpeptide receptors, FPR and FPR2, respectively, may function in vivo as a relay mediating neutrophil migration through the high and low concentration portions of N-formylpeptide gradients.

Key Words: chemoattractant • inflammation • neutrophil • G protein–coupled receptor • phagocyte

G. Barish's present address is University of Michigan School of Medicine, Ann Arbor, MI 48105.

J.K. Hartt's present address is Immunology Department, Harvard Medical School, 200 Longwood Ave., Bldg. D-2, Rm. 137, Boston, MA 02115.

© 1999 The Rockefeller University Press


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