Impaired function of the spermatozoa: Links with mycoplasmal and chlamydial infections

Mycoplasmal and chlamydial infections of the male genital tract have been associated with impairment of the human sperm functionality. However this topic remains doubtful due to contradictory results obtained from several studies around the globe. In this review we will discuss recent evidence from in vitro studies that have confirmed that Mycoplasma hominis, Ureaplasma urealyticum, U. parvum, M. genitalium and/or Chlamydia trachomatis can attach to and invade intact spermatozoa. Moreover we will explore how these bacterial infections can cause impaired sperm function and male infertility. First, bacteria attached to sperm membrane may provoke oxidative stress through release of reactive oxygen species, resulting in lipid peroxidation and reduction of membrane fluidity. Second, chlamydial lipopolysacharide interaction with sperm membrane alters the phosphorylation pattern of citosolic proteins, triggering apoptotic pathways. Third, internalized mycoplasmal and chlamydial cells disrupt the host cell energy production by competing for biosynthetic precursors, thereby altering sperm motility and viability. Fourth, mycoplasmal hydrolytic enzymes (endonucleases, fosfolipases, aminopeptidases) can considerably modify cellular and nuclear organization. Fifth, bacterial surface attachment may mask sperm receptors involved in chemotaxis and oocite recognition, thus impeding fertilization. Sixth, compromise of sperm membrane integrity can lead to exposure of self-antigens and elicitation of an autoimmune response of antisperm antibodies. Finally, we will offer new perspectives for the study of mycoplasmal and chlamydial infections of human spermatozoa.