Sperm are designed to swim through a womanâ€™s cervix, where they travel to the fallopian tubes to fertilize an egg.This journey relies on a number of events, including passing through the cervical mucous.
A protein, named protein beta defensin 126 (DEFB126), acts as a shield that allows sperm to penetrate cervical mucous in its journey to the egg. A new research study has found that men who have mutations in DEFB126, or lack it all together, are more likely to be infertile.
For years, experts have believed that a measure of male fertility is high sperm quality. Quality can be defined as good motility, rapid movement, normal shape, and adequate numbers.
However, researchers have shown that even sperm defective in the DEFB126 protein look healthy under a microscope.
But when DEFB126 defective sperm were added to a cervical mucous-like gel, they were less able to penetrate its barrier than normal healthy sperm. Interestingly, when DEFB126 protein was added to the defective sperm, they regained normal motility through the gel.
The study included sperm from men in the U.S., Britain, Japan, Africa and China. Three-quarters of the men had some level of defect in DEFB126. Birth rates in couples where the man had the most severe defect in DEFB126 were 30% lower than other couples in the study.
Exposing the DEFB126 mutation doesnâ€™t solve all male fertility issues. Stress factors, environmental exposures, and other genetic disorders can act to affect fertility as well.
However, this new knowledge may provide a target for male fertility therapies and help alleviate male fertility issues arising from DEFB126 mutations.