Anti-sperm antibodies (ASAs) have been shown to contribute to male infertility in multiple species but never been examined in male camels. We have developed and evaluated an ELISA assay to specifically detect and quantify ASAs in the serum and seminal plasma of 29 infertile dromedary male camels, which were of two different breeds (Waddah & Majaheem) and three different ages (> 3 to ≤5, ≥5 to ≤7, and >7 years). ASAs were detected in ≥ 80% of the examined animals with considerable individual variation within each group. The serum and seminal plasma ASAs indexes (%) were significantly elevated in the >7 years group compared to the >3 to ≤5 and ≥5 to ≤7 years groups (P ≤ 0.05), and in the ≥5 to ≤7 years group compared to the >3 to ≤5 years group (P ≤ 0.05). Serum and seminal plasma ASAs indexes were significantly higher in the Waddah breed compared to the Majaheem breed (P ≤ 0.05). The sperm motility and viability were significantly higher in the >7 years group compared to the > 3 to ≤5 years and ≥5 to ≤7 years groups (P ≤ 0.05 and P ≤ 0.01, respectively). Significant differences were also observed between the examined two breeds concerning sperm viability and motility with sperm viability being higher in the Majaheem breed (P ≤ 0.05) and sperm motility in the Waddah breed (P ≤ 0.05). Our data demonstrated the presence of ASAs in sera and seminal plasma of infertile dromedary male camels. Our results suggested that age and breed influenced serum and seminal plasma levels of ASAs in male camels. Data presented in the current study highlight the potential role of ASAs in camel infertility; however, more work is needed to determine ASAs' contribution to reproductive challenges in camels.

Background and Aim: Anti-sperm antibodies (ASAs) treatment continued to be neglected. This study aimed to generate ASAs using the testicular sperm aspiration (TSA) rat model, which allowed for investigation of four distinct therapeutic approaches to find potential treatments for ASAs. Materials and Methods: Adult Wistar albino male rats were divided into six equal groups (n = 12). The negative control group underwent scrotal sac surgery without having their testicles punctured. Punctures were made in the remaining 5 groups, with one group left untreated to serve as the positive control group. The remaining 4 groups were treated with either dexamethasone (DEX), azathioprine (AZA), frankincense, or anti-ASAs secondary antibodies. For 10 weeks, serum samples were collected every 2 weeks for specific quantification of ASAs. Testis and epididymis tissues were collected for histopathological analysis. Results: The ASAs concentrations of the positive controls were significantly higher (p ≤ 0.001) than their negative control counterparts during the examined weeks. However, The ASAs indices (%) differed according to the treatment type. While the ASAs indices at the 2nd and 4th weeks in the AZA-treated group were significantly reduced compared to the positive control group (p ≤ 0.001), no significant differences were observed at any of the sample collection week for the DEX-treated rats. The ASAs indices were significantly decreased only at weeks 6 and 8 of treatment in the frankincense-treated group (p ≤ 0.001). In the secondary antibodies-treated group, the antibody indices were significantly decreased in all weeks except for samples collected at week 4 (p ≤ 0.001). The testosterone levels reverted to normal only in TSA rats treated with either Frankincense or secondary antibodies, as they were significantly higher than the positive controls (p ≤ 0.05). Tissue samples from the secondary antibody-treated rats showed a generally normal histological appearance. Conclusion: This study tried to offer realistic therapy suggestions; however, caution should be applied when extrapolating findings from experimental models to meet clinical requirements.