These data are similar to those established for the age-dependent changes of antibodies towards exogenous antigens, suggesting that the 'naturally occurring' antibodies against human spermatozoa are not auto-/isoantibodies.
The genital Chlamydia infection may play a role in the induction of ASA. This is probably a result of the inflammatory process, but not of cross-reactivity between sperm and Chlamydia trachomatis antigens.
The origin of 'natural' anti-sperm antibodies found in fertile humans, virgin girls, and boys before puberty, is quite obscure. One hypothetical mechanism relates their existence to inflammatory gastrointestinal entities: as a result of the disease, cross-reactive antibodies produced against gastrointestinal flora bind spermatozoa. To test this assumption, we evaluated the level of serum sperm antibodies after diarrhoeal infections. Serum samples from 17 patients with shigellosis and 12 patients with salmonellosis were screened for anti-sperm antibodies directed against sperm surface antigens (gelatin agglutination test - GAT, tray agglutination test - TAT, sperm immobilization test - SIT), profound sperm antigens [enzyme-linked immunosorbent assay (ELISA)], and anti-bacterial antibodies (slide agglutination test - SAT) upon diagnosis (group A) and 4-35 days later (group B). The patients from group B demonstrated an increased sperm antibody incidence by GAT (20.7%), TAT (13.8%) and ELISA (31%) when compared to group A and to healthy controls, although statistically significant data were acquired only for the latter group. The absorption of positive sera with bacteria and/or spermatozoa revealed significant reactivity changes in the antibody values by GAT and TAT for shigellosis, and by TAT and ELISA for salmonellosis patients. These data demonstrate increased serum sperm antibody levels in salmonellosis and shigellosis patients.
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