Akademik Veri Yönetim Sistemi
Turk Hijyen ve Deneysel Biyoloji Dergisi, cilt.82, sa.3, ss.409-418, 2025 (Scopus)
Objective: Since stress has become an inseparable aspect of human existence, the interplay between stress and the immune system is a primary focus of research. Despite serotonin being a crucial regulator of the immune and stress systems, its potential involvement in the stress-induced immunological response remains unexamined. This study employed two serotonin receptor antagonists to assess the modulatory influence of serotonin on the immunological response to acute stress. Methods: Fifty-four Wistar albino rats (n=9/group) were allocated into six groups: control (C), acute stress (AS), ondansetron (O), methiothepin (M), acute stress + ondansetron (ASO), and acute stress + methiothepin (ASM). Rats were administered intraperitoneal injections of ondansetron or methiothepin at doses of 2 mg/kg and 0.2 mg/kg, respectively, prior to the introduction of acute stress. Acute stress was induced by a coldimmobilization procedure. Immediately following the stress procedure, the animals were euthanized using exsanguination. A complete blood count was taken, and plasma levels of serotonin, IL-6, and IL-17 were quantified by ELISA. Results: Acute stress significantly decreased leukocyte counts and IL-17 levels relative to the control group (p = 0.003 and 0.002, respectively). Methiothepin had comparable effects on both parameters. On the other hand, neither acute stress nor serotonin receptor antagonists significantly altered IL-6 levels. Nonetheless, when rats were administered a serotonin receptor antagonist and subjected to acute stress (the ASO and ASM groups), the differences in IL6 levels reached statistical significance (p<0.0001). Despite both serotonin antagonists exhibiting comparable effects on immunological response under acute stress, we were unable to observe any alterations in plasma serotonin levels across all groups. Conclusion: These results suggest that the serotonergic system may play a modulatory role in the acute stress-induced immune response and that this modulation is more likely occurring at the receptor level. This phenomenon might be related to desensitization or downregulation of serotonin receptors.