etiopathogenesis of autoimmune responses against sperm

etiopathogenesis of autoimmune responses against sperm

;V. A. Bozhedomov;M. A. Nikolayeva;E. A. Sporish;I. M. Rokhlikov;N. A. Lipatova;I. V. Ushakova;N. S. Loginova;G. T. Sukhikh
andrologiâ i genitalʹnaâ hirurgiâ 2014 Vol. 13 pp. 45-53
491
bozhedomov2014andrologietiopathogenesis

Abstract

The autoimmune reactions against sperm, which are accompanied by the elaboration of antisperm antibodies (AsAb), are one of the causes of male infertility.

Objective: to specify the role of different factors (other than obstruction) in the etiology of male immune infertility.

Subjects and methods. Clinical and laboratory studies were made in 536 males from infertile couples (their age 18–45 years); a control group comprised fertile men whose wives were 8–16 weeks pregnant (n = 82). Their sperms were examined in accordance with the WHO recommendations. AsAbs in the sperm were determined by a MAR test. Oxidative stress was estimated using luminol-dependent chemiluminescence. Chromosome damage was identified from DNA fragmentation by chromatin dispersion in an inert agarose gel, by making a microscopic examination of halo formation after acid DNA denaturation and nuclear protein lysis. The blood levels of interferons (IFN) and their natural and in vitro induced production were determined by the Campbell method. Reproductive tract infections were diagnosed by polymerase chain reaction.

Results. There is a high significant correlation between the quantity of AsAb, on the one hand, and previous orchitis, as well as subclinical testicular injury, on the other hand. There was no correlation between varicocele and AsAb, but in the former, the risk of immune infertility and orchitis increases after injury; varicocelectomy promotes a reduction in AsAb with the higher degree of varicocele and a less marked autoimmune process. AsAbs are observed during Chlamydia infection with the increased production of IFN-γ. Cryptorchidism and orchiopexy, parotitis, epididymitis, herniotomy, chronic bacterial prostatitis, and other potential risk factors for decreased male fertility had no significant impacts on an odds ratio for developing immune infertility. In the majority (41 %) of cases, immune infertility seems to be idiopathic, but it is accompanied by the hyperproduction of reactive oxygen species and DNA damage (fragmentation).

Conclusion. Male immune infertility is multietiological: blood-testis barrier damage, cross reactions with microorganisms, and immunopathological reactions. Autoimmune reactions against sperm can be considered to be both a cause and a sequence of the bad semen quality caused by genetic and different endo- and exogenous factors.

 

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