SOMATOSTATIN MAY PARTICIPATE IN THE ANTIINFLAMMATORY ACTIONS OF GLUCOCORTICOIDS

Glucocorticoids are potent antiinflammatory agents. They inhibit leuko cyte chemotaxis and vascular permeability and generally suppress the e xpression of many inflammatory mediators. Recent reports suggested tha t somatostatin (Sms) had significant immunomodulatory properties in vi tro and in vivo. In this study we examined the effects of glucocortico ids on immunoreactive somatostatin expression in aseptic inflammatory sites of Sprague-Dawley rats given carrageenin sc. The progress of the inflammatory reaction was studied over a 7-h period with respect to t he volume and cellularity of the exudate and the levels of the inflamm atory mediators expressed in the inflammatory site, including immunore active substance P (sP), corticotropin-releasing hormone (CRH), and tu mor necrosis factor-alpha (TNF alpha). Dexamethasone significantly red uced the volume and cellularity of the inflammatory exudates; in paral lel, the levels of immunoreactive sP, CRH, and TNF alpha were signific antly suppressed by this glucocorticoid. In contrast, immunoreactive S ms was stimulated by dexamethasone in a time-dependent fashion. These findings suggest another mechanism for suppression of the inflammatory reaction by glucocorticoids via stimulation of local Sms expression, which occurs in parallel to the inhibition of the local inflammatory m ediators sP, CRH, and TNF alpha.