Reaction to damage of connective tissue in immunoprivileged organ (testis)

Abstract

Microenvironment of sperm and its precursors includes various immune cell populations. This indicates not only their importance for immune privileged state within testes, but it concerns a regulatory role of these structures in performance of the most important physiological functions. Despite sufficient knowledge on the immune privileged state in the organ, the regulatory function are scarcely studied, and existing literature virtually does not cover the issues of local spermatogenesis regulation by various components of testicular microenvironment in the course of their regeneration. Purpose of the present study was to define the reactions of connective tissue in rat testis following traumatic lesion. Materials and methods: the study was carried out in mature male Wistar rats. Experimental animals were divided into 2 groups: intact animals and animals with blunt trauma to the left testicle. The animals were removed from the experiment on the 7th and 30th days. Blunt trauma was simulated by squeezing the organ with forceps with a force of 15 N for 3 seconds. For histological examination, the testes were excised, preparations were made by the standard scheme, stained with hematoxylin/ eosin, toluidine blue (to identify mast cells), and according to Van Gieson (to detect collagen fibers). Distinct components of connective tissue and spermatogenesis were evaluated in testicular preparations. Quantitative indexes were calculated using the ImageJ program. Total testosterone levels in the blood were determined by chemiluminescence technique. Statistical evaluation was performed with Statistica 8.0 software. Comparison of groups was performed using Mann-Whitney test. We have found that restoration of spermatogenesis in the damaged testis did not occur within 30 days after the injury. While the reaction of connective tissue was noted in the both testes, it was more pronounced in the damaged organ, and manifests as changes in testicular microvasculature, stimulation of fibroblastic response, multidirectional effects of mast cells and Leydig cells, depending on the duration of exposure. Changes in various components of microenvironment in the damaged testis led to similar changes in the intact organ. The mechanism of this change is usually associated with effect of antisperm antibodies and development of autoimmune processes, but another possible mechanism for impairment of spermatogenesis in the second paired intact organ may include effects of connective tissue microenvironment upon the spermatogenic epithelial cells.