Absence of a Direct Effect of Recombinant Interleukins and Cultured Peritoneal Macrophages on Early Embryonic Development in the Mousel
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This study found that recombinant interleukins IL-1 and IL-2, as well as activated human peritoneal macrophages, did not directly impair early mouse embryonic development, challenging hypotheses linking these factors to endometriosis-associated infertility.
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Abstract
On the basis of their recent studies, several researchers have suggested that the infertility associated with mild endometriosis is due to the alteration of peritoneal fluid, resulting in impairment of the viability of gametes or embryos. Elevated numbers of macrophages and lymphocytes have been reported in the peritoneal fluid of patients with endometriosis. Interleukin-1 (IL-I) a major product of activated macrophages and Interleukin-2 (IL-2), a product of most activated T-cells, have been postulated to play a role in the infertility associated with this disease, possibly by acting as direct embryotoxic agents. We have exwnined the effect of purified recombinant IL-I and IL-2, which are not species-specific, on in vitro development of mouse embryos. Both interleukins had no effect on development to the blastocyst stage or on early stages of implantation, as measured in vitro by attachment and outgrowth of blastocysts to fibronectin-coated dishes. Moreover, co-culture of mouse embryos with activated human peritoneal macrophages had no effect on embryogenesis. We conclude that neither IL-I, nor other products of human macrophages activated by lipopolysaccharide, nor IL-2 are directly toxic to early mouse embryonic development.
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