Title : Assessment of the role of Uropathogens in reproductive performance of male mice
Abstract:
Infertility is a condition in which conception does not occur even after one year of regular unprotected sexual intercourse. Out of the 15% of the affected couples, the male factor is involved in 40-50% of the infertility cases . Of the various reasons cited for male infertility, the microbial infections have not been given their due because of their asymptomatic nature. Even though the microorganisms could be isolated from semen of both fertile as well as infertile men, yet several reports have surfaced up regarding their greater frequency in semen samples from asymptomatic infertile patients than in those from fertile men. The microorganisms which are most prevalent in semen belong to uropathogens viz. Staphylococcus aureus, Enterococcus faecalis, Escherichia coli, Klebsiella sp, Proteus sp., Pseudomonas sp. and Serratia sp. The presence of these uropathogens in semen has been confirmed by various studies but their role in male fertility is still controversial. These uropathogenic microorganisms can negatively affect the sperm motility leading to immobilization without (SI) or with agglutination (SA) while others do not impede with them at all (NSI-NSA). This can be attributed to either release of secretory factors or direct interactions. Apart from motility, SI/SA microorganisms also impair various other sperm parameters viz. viability, Mg2+-dependent ATPase activity and acrosome reaction. Further, the presence of sperm impairing (SI/SA) uropathogens in threshold number in the male urogenital system lead to reduced reproductive potential of male mice as a consequence of deterioration of process of spermatogenesis and the absence of same in case of NSI-NSA microorganisms highlighting that merely the bacterial colonization is not imperative; rather the sperm impairing property is vital. Moreover, SI/SA microorganisms also increased levels of inflammatory markers i.e. MDA and cytokines, which lead to oxidative stress and tissue injury, further indicating the participation of an additional mechanism i.e. inflammation, in subsequent development of male infertility.