Abstract
Unidentified soluble factors secreted by E. coli, a frequently isolated microorganism in genitourinary infections, have been reported to inhibit mitochondrial membrane potential (ΔΨm), motility and vitality of human spermatozoa. Here we explore the mechanisms involved in the adverse impact of E. coli on sperm motility, focusing mainly on sperm mitochondrial function and possible membrane damage induced by mitochondrial-generated reactive oxygen species (ROS). Furthermore, as lactobacilli, which dominate the vaginal ecosystem of healthy women, have been shown to exert anti-oxidant protective effects on spermatozoa, we also evaluated whether soluble products from these microorganisms could protect spermatozoa against the effects of E. coli. We assessed motility (by computer-aided semen analysis), ΔΨm (with JC-1 dye by flow cytometry), mitochondrial ROS generation (with MitoSOX red dye by flow cytometry) and membrane lipid-peroxidation (with the fluorophore BODIPY C11 by flow cytometry) of sperm suspensions exposed to E. coli in the presence and in the absence of a combination of 3 selected strains of lactobacilli (L. brevis, L. salivarius, L. plantarum). A Transwell system was used to avoid direct contact between spermatozoa and microorganisms. Soluble products of E. coli induced ΔΨm loss, mitochondrial generation of ROS and membrane lipid-peroxidation, resulting in motility loss. Soluble factors of lactobacilli prevented membrane lipid-peroxidation of E. coli-exposed spermatozoa, thus preserving their motility. In conclusion, sperm motility loss by soluble products of E. coli reflects a mitochondrial dysfunction-related membrane lipid-peroxidation. Lactobacilli could protect spermatozoa in the presence of vaginal disorders, by preventing ROS-induced membrane damage.
Highlights
It has been reported that E. coli, a frequently isolated microorganism in genitourinary infections [1], may exert adverse effect on human sperm motility [2,3,4]
As we recently demonstrated, soluble factors produced by a mix of 3 selected strains of lactobacilli (L. brevis CD2, L. salivarius FV2, and L. plantarum FV9), which are effective in treating bacterial vaginosis in the form of vaginal tablets [21], prevented lipid peroxidation of sperm membrane induced in vitro by ferrous ion, preserving sperm motility and vitality [22]
Soluble factors of E. coli produced a decrease in sperm motility which was prevented by lactobacilli
Summary
It has been reported that E. coli, a frequently isolated microorganism in genitourinary infections [1], may exert adverse effect on human sperm motility [2,3,4]. As documented by electron microscopy studies, E. coli exhibits the ability to affect spermatozoa directly via cellular interactions mediated by bacterial fimbrias, interacting with receptors in both the sperm tail and head, leading to sperm adhesion and agglutination [4,5,6,7,8]. These direct effects of E. coli on human sperm motility were found to depend upon the bacterial concentration [4]. In in vitro models of genital tract infection, the addition of leucocytes in the incubation medium enhanced the harmful activity of E. coli on sperm motility [11], by inducing sperm membrane lipid peroxidation [12]
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