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Interleukin I and the glomerular mesangium. II. Monokine stimulation of mesangial cell prostanoid secretion
1Institut für Molekularpharmakologie, Medizinische Hochschule, Hannover, West Germany.
Monocytic (MC) infiltration is a prominent feature of many forms of immune-mediated glomerulonephritis. Through the release of interleukin-1, (IL-1), monocyte/macrophages have been shown to induce the proliferation of mesangial cells and to stimulate the secretion of a glomerular basement membrane-degrading neutral proteinase. In addition, mesangial cells release a cytokine that expresses many of the biologic properties of monocyte IL-1, including stimulation of mesangial cell proliferation. Because many of the actions of IL-1 are mediated by the induction of prostanoid prostaglandin (PG) synthesis, the authors determined the effects of purified macrophage and mesangial IL-1 on the secretion of prostaglandin E (PGE), prostacyclin, and thromboxane. The results indicated that cycling MCs release primarily PGE in response to purified IL-1. The local release by either monocytes or mesangial cells of IL-1 during glomerular inflammation, with subsequent mesangial cell generation of vasodilatory PGE, may be responsible in part for the alterations in the glomerular microcirculation observed in these disorders.
Monocytic (MC) infiltration is a prominent feature of many forms of immune-mediated glomerulonephritis. Through the release of interleukin-1, (IL-1), monocyte/macrophages have been shown to induce the proliferation of mesangial cells and to stimulate the secretion of a glomerular basement membrane-degrading neutral proteinase. In addition, mesangial cells release a cytokine that expresses many of the biologic properties of monocyte IL-1, including stimulation of mesangial cell proliferation. Because many of the actions of IL-1 are mediated by the induction of prostanoid prostaglandin (PG) synthesis, the authors determined the effects of purified macrophage and mesangial IL-1 on the secretion of prostaglandin E (PGE), prostacyclin, and thromboxane. The results indicated that cycling MCs release primarily PGE in response to purified IL-1. The local release by either monocytes or mesangial cells of IL-1 during glomerular inflammation, with subsequent mesangial cell generation of vasodilatory PGE, may be responsible in part for the alterations in the glomerular microcirculation observed in these disorders.