Roles of phospholipase C β2 in chemoattractant-elicited responses

Roles of phospholipase C β2 in chemoattractant-elicited responses

^*Department of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642; and ^†Division of Biology, California Institute of Technology, Pasadena, CA 91125

Abstract

The physiological roles of phospholipase C (PLC) β2 in hematopoiesis, leukocyte function, and host defense against infection were investigated using a mouse line that lacks PLC β2. PLC β2 deficiency did not affect hematopoiesis, but it blocked chemoattractant-induced Ca²⁺ release, superoxide production, and MAC-1 up-regulation in neutrophils. In view of these effects, it was surprising that the absence of PLC β2 enhanced chemotaxis of different leukocyte populations and sensitized the in vivo response of the PLC β2-deficient mice to bacteria, viruses, and immune complexes. These data raise questions about the roles that PLC β2 may play in signal transduction induced by chemoattractants in leukocytes.

Footnotes

↵ ‡ To whom reprint requests should be addressed at: Department of Pharmacology and Physiology, University of Rochester, 601 Elmwood Ave, Box 711, Rochester, NY 14642. e-mail: wud{at}pharmacol.rochester.edu.
Melvin I. Simon
ABBREVIATIONS:

PLC,

phospholipase C;

fMLP,

fMet-Leu-Phe;

IL,

interleukin;

PTx,

pertussis toxin;

MBSA,

methylated bovine serum albumin