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In vitro effect of cetirizine on PGE2 release by rat peritoneal macrophages and human monocytes
Authors:M. Roch-Arveiller  M. Tissot  N. Idohou  G. Sarfati  J. P. Giroud  D. Raichvarg
Affiliation:(1) Département de Pharmacologie, Pavillon Gustave Roussy, CNRS URA 1534, 27 rue du Faubourg St. Jacques, F-75679 Paris Cedex 14, France;(2) Biochimie A2, Hôpital Cochin, 27 rue du Faubourg St. Jacques, F-75679 Paris Cedex 14, France
Abstract:
Cetirizine was first described as a specific anti-H1 molecule displaying potent antiallergic activity. It was later found that its pharmacological properties extended to cellular actions as on eosinophil recruitment at inflammatory sites in allergic patients. Monocytes and macrophages participate in allergic mechanisms, particularly through high affinity H1 and H2 membrane receptors and generation of pro- and anti-inflammatory agents; among them histamine-induced factors, IL-1 and prostanoids are of importance. The aim of this work was to investigate the effect exerted by various concentrations of cetirizine (0.1–10 mgrg/ml) appliedin vitro to human monocytes and peritoneal rat macrophages cultured for 24 h. Peritoneal macrophages were collected either from normal or experimentally inflamed rats. Human monocytes, isolated from peripheral blood, were studied either in a resting state or after stimulation by LPS fromEscherichia coli (1 and 10 mgrg/ml). Cetirizine (10 mgrg/ml) significantly enhanced IL-1 release by human monocytes stimulated by a weak LPS concentration (1 mgrg/ml) but could not modify the maximal increase of IL-1 release induced by 10 mgrg/ml of LPS. It did not exert any effect on resting cells. Cetirizine (0.1–10 mgrg/ml) enhanced PGE2 release by resting human monocytes. Concentrations of 1 and 10 mgrg/ml enhanced PGE2 release by LPS-stimulated monocytes, and by healthy and inflamed rat macrophages. This effect was concentration-dependent. Our findings point to an anti-inflammatory action of cetirizine via PGE2 release and histamine H2 interactions. Cetirizine did not directly modify IL-1 generation by resting monocytes but the IL-1 production observed after LPS stimulation could promote the mechanisms by which PGE2 is released.
Keywords:Cetirizine  Anti H1  PGE2  IL-1  Monocyte/macrophage
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