作者: G. Ménard , V. Turmel , E. Y. Bissonnette
DOI: 10.1111/J.1365-2249.2007.03492.X
关键词:
摘要: Serotonin, well known for its role in depression, has been shown to modulate immune responses. Interestingly, the plasma level of serotonin is increased symptomatic asthmatic patients and use anti-depressants, reduce levels, provokes a decrease asthma symptoms an increase pulmonary function. Thus, we tested hypothesis that affects alveolar macrophage (AM) cytokine production, altering network lung contributing pathogenesis. AMs were treated with different concentrations (10(-11)-10(-9) M) or 5-HT(1) 5-HT(2) receptor agonists 2 h prior stimulation. T helper 1 (Th1) Th2 cytokines, prostaglandin-E(2) (PGE(2)) nitric oxide (NO) measured cell-free supernatants. Serotonin significantly inhibited production tumour necrosis factor (TNF) interleukin (IL)-12, whereas IL-10, NO PGE(2) increased. These immunomodulatory effects mimicked by agonist but not abrogated antagonist, suggesting implication other 5-HT receptors. Inhibitors cyclooxygenase antibody inhibitory stimulatory effect on TNF IL-10 respectively, synthase inhibitor eliminated serotonin-stimulated increase. Furthermore, AM production. results suggest alters through PGE(2). The reduction Th1-type may contribute