Open AccessHistamine induces IL‐6 production by human endothelial cells
Author(s) -
DELNESTE Y.,
LASSALLE P.,
JEANNIN P.,
JOSEPH M.,
TONNEL A. B.,
GOSSET P.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06148.x
Subject(s) - histamine , cell adhesion molecule , histamine h4 receptor , histamine h1 receptor , endothelium , endothelial stem cell , immunology , histamine receptor , tumor necrosis factor alpha , intercellular adhesion molecule 1 , biology , chemistry , endocrinology , microbiology and biotechnology , medicine , histamine h2 receptor , receptor , in vitro , biochemistry , antagonist
SUMMARY Histamine is one of the major mediators implicated in the physiopathology of allergy. On vascular endothelium, histamine mainly induces early effects: an increase in vasopermeability leading to oedema, a release of lipid mediators and a transient expression of P‐selectin. The aim of this study was to evaluate the effects of histamine on adhesion molecule expression and IL‐6 production by human endothelial cells. Histamine did not modulate the expression of intercellular adhesion molecule‐1 (ICAM‐1). vascular cell adhesion molecule‐1 (VCAM‐1) and E‐selectin but induced a transient expression of P‐selectin as previously reported. In addition, histamine increased in a dose‐(from 10 −5 to 10 −3 M) and time‐ (from 4h to 24 h) dependent fashion the IL‐6 synthesis by endothelial cells. Tumour necrosis factor‐alpha (TNE‐α)‐induced IL‐6 production was also potentiated in a dose‐dependent manner by histamine, without modification of the time course of IL‐6 secretion. Moreover, this increase of IL‐6 production induced by histamine was inhibited in a dose‐dependent manner by HI and H2 histamine receptor antagonists (50% inhibition of IL‐6 production at 5 × 10 −4 M and 4 × 10 −5 M, respectively). So histamine induces, besides already well known effects, a late stimulation of endothelial cells, i.e. the production of IL‐6.