Human spermatozoa activated human polymorphonuclear leukocytes (PMN) in the presence of serum. Activation of PMN was studied by measuring the emission of chemiluminescence by the PMN. The amount of chemiluminescence emitted depended on the number of spermatozoa and the serum concentration, and the presence of antibody or complement. Spermatozoa were able to activate PMN in the presence of heat-inactivated serum (only antibody, no complement), serum obtained from a patient with agammaglobulinemia (without antibodies and only complement as opsonin), and in MgEGTA agammaglobulinemic serum (only the alternative pathway of complement intact). In the presence of heat-inactivated agamniaglobulinemic serum no significant chemiluminescence was observed. It was concluded that spermatozoa activate the alternative pathway of complement. Dead spermatozoa were more able to activate PMN than viable spermatozoa.
To gain more insight into a possible detrimental influence of polymorphonuclear granulocytes (PMN) on fertility, PMN were added to spermatozoa and oocytes in the hamster oocyte assay. Addition of 2.5 x 10(6)/ml PMN to the sperm suspension at the start of the first incubation period (capacitation period) resulted in a significant decrease (P less than 0.03) in the number of decondensed sperm-heads per hamster oocyte (the decondensation index). When a concentration of 0.5 x 10(6)/ml PMN was used, no decrease was found. Stimulation of PMN by phorbol myristate acetate (PMA) did not enhance the inhibitory action of PMN. After incubation of oocytes with PMN for 1 h, an almost total inhibition of decondensation was observed. A significant inhibition could also be obtained when unstimulated PMN (2.5 x 10(6] were added at the start often 3 h coincubation period of spermatozoa and oocytes (P less than 0.004). The inhibition by PMN decreased to a nonsignificant level when the hydroxyl radical scavenger thiourea was present. The possible mechanisms by which PMN affect the results of the hamster oocyte assay and the possible implications of the presence of PMN in the genital tract are discussed.
Isolated sperm from normo-, oligo- and astheno-spermic men were incubated for 20 h in medium supplemented with 8% heat-inactivated or untreated human serum, and in medium with heated or untreated serum deficient in complement factor C3. Before and after incubation, sperm motility was assessed by means of a computer-assisted semen analyser. The results did not show significant differences between the motility of sperm incubated in heated or untreated serum. It is concluded that heating of homologous serum is not necessary for preserving sperm motility and in some cases may even be disadvantageous.
Antibody and complement fixation by viable and nonviable spermatozoa were studied by means of immunofluorescence and a hemolytic assay (CH-50). Spermatozoa were incubated in sera from fertile male and female donors and in peritoneal fluid from fertile women undergoing laparoscopy. Nonviable spermatozoa were able to bind antibody or complement from sera and peritoneal fluid. There was no evidence of antibody or complement fixation by viable spermatozoa. The antibodies present in the serum that bind to spermatozoa belong to the IgG and IgM class; in peritoneal fluid, only IgG could be found. Complement fixation occurred via the classical (antibody-mediated) and alternative pathway. Viable spermatozoa possess antigenic properties different from nonviable spermatozoa. The lack of immunological reaction of women to viable spermatozoa and a possible mechanism for immunological infertility is considered.
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