Relationship between an asymptomatic male genital tract exposure to Chlamydia trachomatis and an autoimmune response to spermatozoa.

The relationship between a localized genital tract humoral immune response to Chlamydia trachomatis and the presence of antisperm antibodies on the surface of motile spermatozoa in the ejaculate was examined in 227 asymptomatic male partners of infertile couples with no history of exposure to C.trachomatis. Semen and serum samples were assayed for immunoglobulin (Ig) A and IgG antibodies to C.trachomatis by enzyme-linked immunosorbent assay employing a recombinant Chlamydia-specific lipopolysaccharide fragment (Medac, Hamburg, Germany), while motile spermatozoa were tested for bound autoantibodies by immunobead binding. Semen samples from 24.7 and 10.9% of the men were positive for IgA and IgG antibodies to C.trachomatis respectively. In comparison, antichlamydial IgA was less prevalent in sera (14.5%) than in semen (P = 0.01), while antichlamydial IgG was most prevalent (21.5%) in sera (P = 0.003). In 75.0% of the men with antichlamydial IgA in their semen, this antibody was undetectable in sera obtained at the time of semen collection. Conversely, 84.0% of the men with seminal antichlamydial IgG were also IgG seropositive. Antisperm IgG and/or IgA were detected on motile spermatozoa from 16.3% of the men; their occurrence was strongly correlated with the presence of antichlamydial IgA in semen (P < 0.0001). Weaker associations between antisperm antibodies and either seminal IgG antibodies to C.trachomatis (P = 0.01) or circulating IgA and IgG antichlamydial antibodies (P = 0.03) were also observed. Men with antichlamydial IgA in their semen had a lower median sperm count (82 versus 144 x 10(6)/ml) than those men without (P = 0.003); sperm morphology and motility were comparable in both groups. These data suggest that asymptomatic male genital tract exposure to C.trachomatis is a frequent event among this population and that the presence of a humoral immune response to this organism is correlated with the development of an autoimmune response to spermatozoa.