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How Does Orchitis Trigger Infertility?

Macrophages, lymphocytes, and mast cells in the Leydig cells of mammalian testis participate in immune monitoring and regulation of testicular immune homeostasis. The supporting cells in seminiferous tubules provide essential nutrients and high concentration androgen environment for spermatogenic cells, form blood-testis barrier, and phagocytize apoptotic spermatogenic cells and debris.
Under normal conditions, T cells are the main lymphocyte in testis, and CD4 + and CD8 + are half. In infective orchitis, macrophages are activated and secrete more inflammatory factors. Inflammatory factors can affect male fertility in many ways, directly or indirectly enhance the killing activity of natural killer (NK) cells and cytotoxic lymphocyte (CTL) cells. It can also regulate spermatogenesis by affecting the secretory function of Sertoli cells.
In the early stage of infection, macrophages, and spermatogenic cells secrete high levels of TNF - α, which limits the spread of bacteria. In the late stage of infection, the bactericidal activity of macrophages was very low, but a high concentration of TNF - α could be detected.
TNF - α is related to the progress of the disease. It can increase the permeability of endothelium, make lymphocytes easily invade testis, stimulate the paracrine and autocrine of T cells, and macrophages.
Sertoli cells are one of the main somatic cells in testis. They synthesize androgen binding protein (ABP), form the blood-testis barrier, and form the microenvironment for spermatogenesis. Fas / FasL system plays an important role in the physiological development and pathological changes of the testis.

The Sertoli cells express TNF - α receptors. TNF - α can induce the mouse Sertoli cells to express Fas in vitro, which can be activated by the FasL effect cells, leading to the apoptosis of Sertoli cells and destroying the blood-testis barrier. The expression of Sertoli cells induced by inflammatory factors can promote the adhesion between immunocompetent cells and Sertoli cells and participate in the pathological process of orchitis.

When infected by cells, pathogenic bacteria can reduce sperm motility, increase the number of abnormal sperm (including agglutination effect), reduce the ability of sperm to pass through the cervix, and change the biochemical environment of seminal plasma, thus having adverse effects on sperm function.
When the reproductive tract is inflamed, the increase of leukocyte numbers can significantly reduce the total number of sperm, sperm viability, sperm motility speed, and a total number of active sperm.
The increased level of ROS in leukocytes can attack the sperm cell membrane and cause lipid peroxidation, which is conducive to the activation of phospholipase A2, the production of lysophospholipin, the destruction of lipid in the sperm cell membrane and the loss of sperm viability.
The inflammatory damage of orchitis can damage the blood-testis barrier, induce the body to produce an active immune response to its own sperm, and produce an anti-sperm antibody (AS-AB), leading to infertility.

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