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A step sensitive to pertussis toxin and phorbol ester in human neutrophils regulates chemotaxis and capping but not phagocytosis
Author(s) -
Lad Pramod M.,
Olson Charles V.,
Grewal Iqbal S.
Publication year - 1986
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(86)80517-8
Subject(s) - chemotaxis , pertussis toxin , phagocytosis , opsonin , receptor , cholera toxin , platelet activating factor , calcium , chemistry , phorbol , microbiology and biotechnology , protein kinase c , biology , biochemistry , signal transduction , g protein , immunology , organic chemistry
Treatment of human neutrophils with pertussis toxin (PT) abolishes chemotaxis in response to either platelet‐activating factor (PAF) or f‐Met‐Leu‐Phe (FMLP), and capping induced via the concanavalin A (Con A) receptor. These functional effects are accompanied by the inhibition of calcium mobilization by PAF, FMLP and Con A. The agent phorbol 12‐myristate‐13‐acetate (PMA) also inhibits chemotaxis and capping as well as calcium mobilization by these receptors. In sharp contrast, neither PT, cholera toxin (CT), nor PMA, inhibits the phagocytosis of non‐opsonized and opsonized Candida albicans , sheep erythrocytes or fluorescent latex beads. Our results suggest that receptor‐initiated chemotaxis and capping involve a step that is sensitive to PT and PMA, and that phagocytosis is not regulated in a similar fashion.