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Virus‐Induced Enhancement of Arachidonate Metabolism by Bovine Alveolar Macrophages In Vitro
Author(s) -
Laegreid W.W.,
Taylor S.M.,
Leid R.W.,
Silflow R.M.,
Evermann J.R.,
Breeze R.G.,
Liggitt H.D.
Publication year - 1989
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.45.4.283
Subject(s) - biology , pulmonary alveolus , arachidonic acid , metabolite , zymosan , lipoxygenase , virus , in vitro , metabolism , alveolar macrophage , macrophage , in vivo , biochemistry , enzyme , immunology , microbiology and biotechnology
Virus infection of alveolar macrophages both in vivo and in vitro has been associated with a variety of changes in cellular function. Some of these changes are identical to the effects that arachidonate‐derived mediators, prostaglandins, leukotrienes, and hydroxyeicosatetraenoic acids, have on macrophage function. Virus infection of macrophages has been previously shown to increase the output of some arachidonate metabolites, most notably PGE 2 . However, the effect of virus infection on arachidonate metabolism in general has not been well described. In our experiments, primary cultures of alveolar macrophages obtained from normal cattle by bronchoalveolar lavage, were infected in vitro with parainfluenza type 3 virus. At days 0 to 4 post‐infection (p.i.) these cells were labelled with 3 H‐arachidonic acid and stimulated with either serum‐coated zymosan, the calcium ionophore A23187, or phorbol myristate acetate. The complete spectrum of arachidonate‐derived metabolites was determined by reverse‐phase high performance liquid chromatography with UV and on‐line radiometric monitoring of column eluant. The total output of metabolites of arachidonic acid by virus‐infected alveolar macrophages was increased over that of noninfected controls (with all stimuli tested) by day 4 p.i. ( P ≤ 0.05). The production of metabolites by the cyclooxygenase, 12‐and 5‐lipoxygenase enzyme systems was significantly increased, as was the release of 3 H‐arachidonate. The lack of stimulus specificity and the increases in arachidonate release suggest that greater substrate availability, due either to increased phosphollpase activity or direct virus‐membrane interaction, may be responsible for the virus‐induced enhancement of metabolite output.