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Interleukin-2 production in whole blood cell cultures of women undergoing controlled ovarian hyperstimulation for assisted reproduction technology cycles.

作者信息

Orvieto Raoul, Leites Tatiana, Abir Ronit, Bar Jacob, Yoeli Rakefet, Feldberg Dov, Fisch Benjamin

机构信息

Department of Obstetrics and Gynecology, Rabin Medical Center, Petah Tiqva and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

出版信息

Am J Reprod Immunol. 2003 Sep;50(3):220-3. doi: 10.1034/j.1600-0897.2003.00061.x.

Abstract

PROBLEM

To determine whether human chorionic gonadotropin (hCG) modulates the in vitro release of interleukin (IL-2) from human peripheral lymphocytes and monocytes derived from patients undergoing controlled ovarian hyperstimulation (COH).

METHOD OF STUDY

A large university-based IVF unit was used for the study. Blood was drawn thrice from 12 women undergoing our routine IVF long gonadotropin-releasing-hormone-analog protocol during the COH cycle: (1) day on which adequate suppression was obtained (Day-S); (2) day of or prior to hCG administration (Day-hCG); and (3) day of ovum pick-up (Day-OPU). At each point of time, blood was tested for sex-steroid levels and then cultured for 72 hr either without (control-culture) or with hCG (hCG-culture) or with mitogenic stimulation by phytohemagglutinin (PHA-culture). The culture-medium supernatants were tested for IL-2 levels with a commercial sandwich enzyme-linked immunoassay.

RESULTS

Whole blood culture IL-2 levels increased significantly during COH until peak E2, and then decreased significantly after hCG administration. IL-2 levels were decreased in the control- and PHA-culture media on Day-OPU compared with Day-hCG. There were no significant correlations between IL-2 levels in the culture media and serum estradiol, progesterone or human chorionic gonadotropin levels.

CONCLUSION

Apparently, hCG attenuates IL-2 production by mononuclear cells with and without mitogenic stimulation, irrespective of the estradiol level. This suggests that hCG may indirectly modulate the inflammatory response, resulting in the ovarian hyperstimulation syndrome.

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