Direct effect of macrophage migration inhibitory factor on sperm function: possible involvement in endometriosis-associated infertility

Fertil Steril. 2007 Oct;88(4 Suppl):1240-7. doi: 10.1016/j.fertnstert.2007.04.002. Epub 2007 Jul 20.

Abstract

Objective: To evaluate the effect of macrophage migration inhibitory factor (MIF) on sperm capacitation, a maturational process that occurs in the female reproductive tract and enables spermatozoa to become fully competent at fertilizing the oocyte.

Design: Incubation of Percoll-washed spermatozoa with varying concentrations of human recombinant MIF or fetal cord serum (positive control).

Setting: Human reproduction research laboratories.

Intervention(s): Fresh semen samples obtained from healthy volunteers after a minimum of 2 days of sexual abstinence.

Main outcome measure(s): Protein tyrosine phosphorylation by Western blotting, the acrosomal status upon binding to the Pisum sativum agglutinin conjugated to fluorescein isothiocyanate, and sperm motility by computer-assisted sperm analysis.

Results: MIF displayed a dose-dependent effect on the phosphotyrosine content of p105 and p81, the two major tyrosine-phosphorylated proteins associated with human sperm capacitation. A significant induction of tyrosine phosphorylation was seen at 2 ng/mL of MIF for both p105 and p81, but a trend for a down-regulation of the basal tyrosine phosphorylation level was noted at elevated concentrations (12-24 ng/mL). MIF pretreatment of spermatozoa resulted in a dose-dependent change in the acrosome reaction induced by the Ca(2+) ionophore A23187. After being increased at 1-4 ng/mL MIF with a statistically significant effect observed at 4 ng/mL, the acrosome reaction gradually decreased and fell below the control levels at higher concentrations. Furthermore, a significant decrease in the motility of spermatozoa was observed after exposure to an elevated concentration of MIF (12 ng/mL).

Conclusion(s): The present data indicate that MIF may play a physiological role in sperm capacitation but may have deleterious effects on sperm function at abnormal pathophysiological levels, which suggests a role in endometriosis-associated infertility.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Dose-Response Relationship, Drug
  • Endometriosis / etiology
  • Endometriosis / metabolism*
  • Female
  • Humans
  • Infertility, Female / etiology
  • Infertility, Female / metabolism*
  • Macrophage Migration-Inhibitory Factors / adverse effects
  • Macrophage Migration-Inhibitory Factors / pharmacology*
  • Macrophage Migration-Inhibitory Factors / physiology
  • Male
  • Sperm Capacitation / physiology*
  • Spermatozoa / physiology*

Substances

  • Macrophage Migration-Inhibitory Factors