Endometritis and Fibrosis: An Evolving Story

Dear Colleagues,

Natural breeding and artificial insemination induce a physiological endometrial response, resulting in inflammatory cell migration into the uterus. In many species, innate and adaptive immune mechanisms are essential for the physiological regulation of uterine function. This interplay among inflammatory cells orchestrates endometrial inflammatory response and remodeling events. Pathogenesis of endometritis is very complex, bridging the action of steroid hormones, eicosanoids, cytokines, growth factors, antioxidants, and others. Physiological endometritis differs among species, depending on semen deposition location, reproductive tract anatomy, and other species specificities. In species with vaginal semen deposition, post-breeding endometritis is reduced, while species with intrauterine semen deposition mount an exuberant physiological endometrial reaction. Seminal plasma induces and controls the inflammatory response. Failure of defense mechanisms in the reproductive tract can induce pathological persistent endometritis or metritis. Persistence of endometrial inflammation leads to pro-fibrotic factor release, collagen deposition, and fibrosis, causing uterine failure and infertility. Each species has its own reproductive strategy. As such, knowledge of similar pathways can improve the assisted reproduction outcome by increasing fertility rates in different species. Thus, this Topical Collection aims to gather sound knowledge that will help to provide new treatments for pathological endometritis and avoid endometrial degenerative changes.

Prof. Dr. Jordi Miró Roig
Dr. Graça Ferreira Dias
Collection Editors

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