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PMID: 474719 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

A possible role of arachidonic acid in human neutrophil aggregation and degranulation.

The American journal of pathology ·Vol. 96 ·No. 3 ·1979-09-00 ·Pages 799-810

O'Flaherty JT, Showell HJ, Ward PA, Becker EL

Abstract

Chemotactic factors stimulate neutrophils to aggregate and, in the presence of cytochalasin B, to degranulate. Recently, the authors found that arachidonic acid also stimulates human neutrophils to aggregate but does not stimulate cytochalasin-B-treated or untreated cells to degranulate. In this report the authors examined the effect of three blockers of arachidonic acid metabolism on these cellular responses. It was found that the arachidonic acid analog 5,8,11,14-eicosatetraynoic acid and indomethacin, but not aspirin, inhibited no only the arachidonic-acid-induced aggregation response but also the degranulation responses evoked by C5a or a synthetic oligopeptide chemotactic factor. These results suggest that arachidonic acid may be a precursor of bioactive metabolites that stimulate the aggregation and foster the degranulation responses of neutrophils. Thus, these metabolites may be mediators of neutrophil function. Agents that block their formation may thereby inhibit aggregation and degranulation.

MeSH Terms
5,8,11,14-Eicosatetraynoic Acid/pharmacology Arachidonic Acids/metabolism,physiology Aspirin/pharmacology Cell Movement/drug effects Cytoplasmic Granules/ultrastructure Humans In Vitro Techniques Indomethacin/pharmacology Neutrophils/drug effects,ultrastructure
Chemicals
Arachidonic Acids 5,8,11,14-Eicosatetraynoic Acid Aspirin Indomethacin
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
O'Flaherty J T
Showell H J
Ward P A
Becker E L
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40 references, click to expand
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Article Info
Journal
The American journal of pathology
Abbr.
Am J Pathol
ISSN
0002-9440
Published
1979-09-00
Pages
799-810
Language
English
Region
United States
NLM ID
0370502
PMCID
PMC2042398
Subset
IM
External Links
PubMed source PMC Full Text View journal details
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