Gonadotropin‐releasing hormone analogues lead to pro‐inflammatory changes in <scp>T</scp> lymphocytes

Abstract

PROBLEM: We aimed to investigate the effect of gonadotropin-releasing hormone (GnRH) analogues on T-cell immunity. METHOD OF STUDY: TNF-α(+) -, INF-ɣ(+) -, IL-10(+) -, and IL-17(+) -expressing T cells in peripheral blood mononuclear cells (PBMCs) were treated with various concentrations (0.1, 1, 5, and 10 μm) of GnRH agonist (buserelin acetate) and antagonist (cetrorelix acetate) for 4 hours in vitro and they were analyzed with flow cytometry. RESULTS: TNF-α(+) /IL-10(+) T helper (TH) cell ratios were increased in PBMCs treated with 1, 5, and 10 μm GnRH agonist when compared to controls (P=.006, P=.014 and P=.030, respectively). IFN-ɣ(+) /IL-10(+) TH cell ratios were significantly increased with 0.1, 1, 5, and 10 μm GnRH agonist as compared with controls (P=.046, P=.004, P=.013, and P=.011, respectively). TNF-α(+) TH cell levels, and IFN-γ(+) /IL-10(+) TH cell ratios were significantly different (P<.001 and P<.004, respectively) between GnRH agonist- and antagonist-treated cells. CONCLUSION: GnRH analogues induce pro-inflammatory TH1 shift in T-cell immunity, in vitro. GnRH treatment during assisted reproductive technology cycle might explain a possible cause of inflammatory flare in women with inflammatory conditions.