Aggregation of macrophages by a human lymphokine (MAgF). Role of the eicosanoid system

Peritoneal exudate cells aggregate when exposed to the lymphokine Macrophage Aggregating Factor (MAgF). The role of prostaglandins in the aggregation of these cells has been investigated with a quantitative assay. Results are discussed in the context of the mode of action of the migration inhibiting...

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Bibliographic Details
Published inJournal de pharmacologie Vol. 14; no. 4; p. 473
Main Authors Rouveix, B, Larno, S, Lechat, P
Format Journal Article
LanguageFrench
Published France 01.10.1983
Subjects
Anti-Inflammatory Agents - pharmacology
Arachidonic Acid
Arachidonic Acids - pharmacology
Cell Aggregation - drug effects
Humans
In Vitro Techniques
Lymphokines - pharmacology
Macrophage-Activating Factors
Macrophages - drug effects
Prostaglandins - physiology
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Summary:Peritoneal exudate cells aggregate when exposed to the lymphokine Macrophage Aggregating Factor (MAgF). The role of prostaglandins in the aggregation of these cells has been investigated with a quantitative assay. Results are discussed in the context of the mode of action of the migration inhibiting factor (MIF) and of the other non immune aggregating stimuli such as C5a and fMLP. Prostaglandins E1, E2, and F2 alpha alone did not cause aggregation of macrophages but partially inhibited the MAgF aggregation of macrophages and this effect was not different from the one obtained with MAgF. MAgF, calcium ionophore A23187 and arachidonic acid induced aggregation were blocked by 5, 8, 11, 14-eicosatetraynoic acid, an inhibitor of arachidonic acid metabolism, by indomethacin (10(-4), 10(-6) M) by corticosteroids (dexamethazone, methylprednisolone, hydrocortisone) but not by aspirin (10(-2), 10(-4) M) nor by phenylbutazone (10(-4), 10(-5) M). These results suggest a causal relationship between MAgF induced macrophage aggregation and that due to other stimuli with respect to the derivatives of arachidonic acid. The lipoxygenase pathways metabolites stimulate aggregation whereas the cyclo-oxygenase pathways metabolites inhibit it.
ISSN:0021-793X