Role of inflammatory mediators in the development of endometrosis in mare

Equine endometrosis is a chronic degenerative condition with progressive fibrosis that forms in the endometrial stroma and around the endometrial glands. Equine endometrosis causes histological changes and alterations in the secretory function of endometrial cells. These alterations lead to changes in the endometrium and early pregnancy dysfunction. Thus, this condition is one of the main causes of subfertility in mares, resulting in enormous economic losses to the horse-breeding industry. In general, fibrosis is characterized by excessive deposition of extracellular matrix (ECM) components. It destroys normal tissue architecture and compromises tissue function. The cellular and molecular events associated with the development of tissue fibrosis are complex and poorly understood. In recent years, research has been carried out on the involvement of immune cells and their products in the pathogenesis of endometrosis in mares. These studies focused mainly on the role of cytokines, such as transforming growth factor (TGF)-beta 1, interleukin (IL) 6, IL-1 beta, prostaglandin (PG), and components of neutrophil extracellular traps (NET), such as myeloperoxidase, cathepsin G, and elastase, in the most important processes associated with the development of endometrosis. The results showed that TGF-beta 1, IL-1 beta, IL-6, and PGs act on myofibroblast differentiation, fibroblast proliferation, deposition of ECM protein, and expression of matrix metalloproteinases (MMPs), and their inhibitors. It suggests their involvement in processes associated with pathological endometrial remodeling. Moreover, the response of endometrial tissue to selected factors changes according to the stage of endometrosis. The action of inflammatory mediators on processes related to the development of fibrosis shows a connection between inflammation and endometrosis.