Relación entre infertilidad masculina e infección genitourinaria por micoplasmas: Una actualización / Relationship between male infertility and genitourinary mycoplasma infection: An update

Por más de 30 años se ha sugerido que las infecciones seminales causadas por micoplasmas promueven el deterioro de la funcionalidad de los espermatozoides humanos. Sin embargo, los estudios al respecto han mostrado resultados contradictorios. En esta revisión presentamos las evidencias recientes de estudios in vitro que confirman que Mycoplasma hominis, Ureaplasma urealyticum, U. parvum y M. genitalium pueden adherirse e invadir los espermatozoides humanos viables y móviles. Así mismo discutiremos cómo estas infecciones pueden causar: a) estrés oxidativo en los espermatozoides; b) interrupción de los mecanismos de producción de energía que alteran la movilidad y viabilidad espermática; c) desorganización de la estructura nuclear y celular por efecto de las endonucleasas, fosfolipasas y aminopeptidasas bacterianas; d) enmascaramiento de los receptores quimiotácticos y obstaculización de la fecundación, y e) compromiso de la integridad de la membrana espermática, con exposición de autoantígenos y respuesta autoinmune.

It has been suggested for more than 30 years that seminal infections caused by mycoplasmas provoke impairment of the human sperm functionality. However, the studies have shown conflicting results. This review presents recent evidence from in vitro studies that confirm adherence and invasiveness toward human spermatozoa by Mycoplasma hominis, Ureaplasma urealyticum, U. parvum and M. genitalium. We discuss how those infections can cause: a) sperm oxidative stress; b) disruption of energy production mechanisms that lead to impaired sperm motility and viability; c) disturbance of nuclear and cellular organization by effect of bacterial endonucleases, phospholipases and aminopeptidases; d) masking of chemotactic receptors and obstruction of fertilization, and e) compromise of sperm's membrane integrity, with exposure of self-antigens and auto-immune responses.

Mycoplasma hominis attaches to and locates intracellularly in human spermatozoa.

BACKGROUND: The study of sperm-mycoplasma interaction has been focused on the effects of infection on sperm quality, but few studies have reported the direct interaction of this bacterium with spermatozoa. METHODS: Selected populations of viable, motile and infection-free human spermatozoa from three healthy men were incubated with 15-480 multiplicity of infection (MOI) units of DiIC18-labelled Mycoplasma hominis. Cells were analyzed by means of confocal microscopy and by the eosin-Y dye exclusion test between 10 min and 24 h post-infection. RESULTS: As early as 10 min post-infection, clusters of M. hominis were seen attached to the sperm head, midpiece or tail. Mycoplasma showed an approximately 2.5-4.5-fold higher interaction with sperm head or tail than with midpiece. Sequential sectioning of infected spermatozoa revealed the intracellular location of M. hominis within cytosolic spaces of head and midpiece regions. A minor proportion of infected spermatozoa showed bent or coiled tails, and/or midpiece thickening. Sperm viability was not altered by M. hominis infection. CONCLUSIONS: These results provide specific and conclusive evidence of M. hominis attachment and invasiveness towards human sperm cells, which seems not to affect their viability, suggesting that a short-term M. hominis interaction with spermatozoa results in non-apparent or subtle damage, but might have implications for long-term male or couple's fertility.

Ultrastructural alterations in human blood leukocytes induced by porcine circovirus type 1 infection.

BACKGROUND: Swine infectious pathogens, especially viruses, represent a potential public health risk associated with the use of pig tissues for xenotransplantation in humans. We hypothesized that porcine circovirus type I (PCV-1) may infect human mononuclear cells, resulting in ultrastructural alterations of the target cells. METHODS: Transmission electron microscopy was used for evaluating ultrastructural alterations of human cells exposed to a PCV-infected PK15 cell line. A polymerase chain reaction (PCR) assay and fluorescence in situ hybridization (FISH) were developed for detecting PCV-1 in human mononuclear cells. RESULTS: Morphological alterations of the human T cells exposed to PCV PK15 showed ''boomerang-shaped'' intracytoplasmic inclusions. Nucleocapsids appeared free, close to the nucleus, or contained into cytoplasmic vacuoles. Virions were observed near the surface of the human cells. A considerable number of mature virions and immature forms could be observed in the human cells that had a completely intact nuclear membrane with no alteration in the disposition of chromatin. PCV-1 particles were identified budding into typical Golgi saccules and vacuoles. Virions sized up to 23 nm in diameter, and appeared in the nucleus and in the periphery of the cellular core. PCV-1 infection was detected on CD4+, CD8+, CD14+, CD19+, and CD56+ human cells by PCR assay and FISH. CONCLUSIONS: These results suggest that PCV has the capability of infecting human leukocytes in vitro, and should be considered a potential risk of viral transmission during xenotransplantation.