Effects of Gonadotropin‐Releasing Hormone Agonist (GnRHa) and Ovariectomy on Leukocyte Subpopulations in Rats With Autotransplanted Endometrium

Hidehiko Matsubayashi, Kenichi Iwasaki, Tetsuo Maruyama, Nobuaki Ozawa, T. Nemoto, Shinya Iwasaki, Wen‐Shu Sun, Wen-Shu Sun, Kazumi Nakazawa, Shiro Nozawa, Tsunehisa Makino
In: American Journal of Reproductive Immunology · 1996 · vol. 36(1) , pp. 40–48 · doi:10.1111/j.1600-0897.1996.tb00137.x · PMID:8831900 · W2034339637
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GnRH agonist and ovariectomy reduced ectopic endometrial growth, correlating with increased natural killer cells and macrophages in rats, suggesting a hypoestrogenic state influences these immune cell populations.

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Abstract

PROBLEM: To determine the effect of estrogen deficiency on populations of immune cells in rats with autotransplanted endometrium. METHOD OF STUDY: Autologous endometrial segments were implanted in the peritoneum of rats. Leukocyte subsets in the peripheral blood (PB) and peritoneal fluid (PF) of autotransplanted rats treated with gonadotropin-releasing hormone agonist (GnRHa) or ovariectomy were analyzed by flow cytometry. RESULTS: Endometrial growth was suppressed in association with increases in natural killer (NK) cells and macrophages in rats treated surgically or medically after endometrial implantation compared with autotransplanted-only rats. Normal rats treated with GnRHa showed no significant alterations in PB and PF leukocyte subsets, even in NK cells and macrophages, compared with untreated normal rats. CONCLUSIONS: Data suggest that GnRHa itself did not have an immunomodulating effect when rats were treated for 3 weeks, but that a hypoestrogenic state reduced the size of the ectopic endometrium in association with increases in NK cells and macrophages. Our findings support the hypothesis that ectopic endometrial cells may release immunosuppressive factors.

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