Silent chronic inflammation of genital tract (CIGT) is considered as a major contributing factor to male fertility disorders. Within CIGT, inflammatory cytokines such as TNF‐α might induce spermatozoal apoptosis, which in turn has been shown to have a negative influence on the sperm‐oocyte penetration capacity. Thus, the aim of this study was to investigate spermatozoal apoptosis in patients with fertility disorders and signs of CIGT. Apoptosis of spermatozoa was determined by expression of annexin V using flow cytometry. Apoptotic spermatozoa were further discriminated from necrotic spermatozoa by 7‐amino‐actinomycin (7AAD). Ejaculates of patients showing signs of CIGT (P‐CIGT) such as high polymorphonuclear (PMN) elastase were compared to control ejaculates of patients lacking signs of CIGT (CON). Thereby we detected a significant correlation between PMN elastase and TNF‐α in the seminal plasma and apoptotic spermatozoa. Furthermore, we demonstrated a significantly higher percentage of apoptotic spermatozoa in the ejaculate of P‐CIGT compared to CON. Interestingly, a significantly higher percentage of apoptotic spermatozoa was detected in the swim‐up fraction demonstrating motility of apoptotic spermatozoa. This is in line with the missing correlation of apoptotic spermatozoa and motility. In conclusion, patients with signs of CIGT display high numbers of apoptotic spermatozoa with progressive motility, which might have an impact on reproductive techniques such as intrauterine insemination or in‐vitro fertilisation.

Background: Because of the infrequence of salivary gland tumours and their complex histopathological diagnosis it is still difficult to exactly predict their clinical course by means of recurrence, malignant progression and metastasis. In order to define new proliferation associated genes, purpose of this study was to investigate the expression of human α-defensins (DEFA) 1/3 and 4 in different tumour entities of the salivary glands with respect to malignancy. Methods: Tissue of salivary glands (n=10), pleomorphic adenomas (n=10), cystadenolymphomas (n=10), adenocarcinomas (n=10), adenoidcystic carcinomas (n=10), and mucoepidermoid carcinomas (n=10) was obtained during routine surgical procedures. RNA was extracted according to standard protocols. Transcript levels of DEFA 1/3 and 4 were analyzed by quantitative realtime PCR and compared with healthy salivary gland tissue. Additionally, the proteins encoded by DEFA 1/3 and DEFA 4 were visualized in paraffin-embedded tissue sections by immunohistochemical staining. Results: Human α-defensins are traceable in healthy as well as in pathological altered salivary gland tissue. In comparison with healthy tissue, the gene expression of DEFA 1/3 and 4 was significantly (p<0.05) increased in all tumours – except for a significant decrease of DEFA 4 gene expression in pleomorphic adenomas and a similar transcript level for DEFA 1/3 compared to healthy salivary glands. Conclusions: A decreased gene expression of DEFA 1/3 and 4 might protect pleomorphic adenomas from malignant transformation into adenocarcinomas. A similar expression pattern of DEFA-1/3 and -4 in cystadenolymphomas and inflamed salivary glands underlines a potential importance of immunological reactions during the formation of Warthin’s tumour.

Epididymitis is an epididymal inflammation that may lead to male infertility. Dendritic cells (DCs) and myeloid differentiation primary response gene 88 (Myd88) were associated with epididymitis in rodents. However, the functions of Myd88 on epididymal DCs remain unclear. This study investigated the role of Myd88 in DCs for epididymitis. The Myd88 signaling pathway, phenotypes of DC subsets, and cytokines were investigated in lipopolysaccharide (LPS)-induced epididymitis in mice. CRISPR-Cas9 was used to knockout Myd88 in bone-marrow-derived dendritic cells (BMDCs) and immortalized mouse epididymal (DC2) cell line. In the vivo experiments, levels of the proinflammatory cytokines IL-1α, IL-6, IL-17A, TNF-α, IL-1β, MCP-1, and GM-CSF, mRNA for MyD88 related genes, and the percentages of monocyte-derived DCs (Mo-DCs) were significantly elevated in mice with epididymitis. In the vitro experiments, LPS significantly promoted the apoptosis of BMDCs. In addition, the concentration of inflammatory cytokines in BMDCs and DC2s were increased in the LPS group, while decreasing after the knockout of Myd88. These findings indicate that Myd88 on DCs is involved in the inflammation of epididymitis in mice, which may be a potential target for better strategies regarding the treatment of immunological male infertility.