Inflammation and fertility in the mare

Abstract

Contents A transient uterine inflammation post‐breeding is a normal physiological reaction in the mare, and it is believed that the inflammatory response is necessary to eliminate bacteria and excess spermatozoa introduced into the uterine lumen. A tight balance between multiple pro‐ and anti‐inflammatory factors is required for resolving the breeding‐induced inflammation within 24–36 hr in the reproductively healthy mare, whereas a subpopulation of mares is susceptible to development of a persistent infection that can interfere with fertility. The aetiology of persistent endometritis can be either bacterial or semen‐induced and both scenarios can threaten the establishment of pregnancy. Several factors associated with susceptibility to persistent endometritis have been identified including altered innate immune response in the early inflammatory process, reduced myometrial contractions and impaired opsonization; however, the pathogenesis to susceptibility has not been fully elucidated. Current research focuses on the initial hours of uterine inflammatory responses to semen and bacteria, and potential treatments to modify this altered innate immune response. An increased understanding of the mechanisms involved in the disease progression is necessary to improve the treatment and management of these mares. This review attempts to summarize the current knowledge of the uterine inflammatory and immunological responses to breeding‐induced endometritis, persistent breeding‐induced endometritis (PBIE) and bacterial endometritis in the mare.

The Healthy and Diseased Equine Endometrium: A Review of Morphological Features and Molecular Analyses

“…A transient endometritis after mating or insemination is a physiological reaction and has the function to eliminate excess spermatozoa, seminal plasma, cellular debris, and bacteria [12]. Similar to after bacterial infection, the inflammatory response is characterized by the production of proinflammatory cytokines, i.e., interleukin (IL) 1β, IL8, and IL6 and tumor necrosis factor-α within 2 h [60]; recruitment of neutrophils within 30 min to 2 h [10,11,74]; and an influx of T cells within 6 h [75]. Neutrophils release prostaglandin F2α, resulting in myometrial contractions to remove intrauterine inflammatory contents [11,74].…”

“…Similar to after bacterial infection, the inflammatory response is characterized by the production of proinflammatory cytokines, i.e., interleukin (IL) 1β, IL8, and IL6 and tumor necrosis factor-α within 2 h [60]; recruitment of neutrophils within 30 min to 2 h [10,11,74]; and an influx of T cells within 6 h [75]. Neutrophils release prostaglandin F2α, resulting in myometrial contractions to remove intrauterine inflammatory contents [11,74]. In addition, anti-inflammatory cytokines, i.e., IL10 and IL1RN, increase within 6 h [60,74].…”

“…Neutrophils release prostaglandin F2α, resulting in myometrial contractions to remove intrauterine inflammatory contents [11,74]. In addition, anti-inflammatory cytokines, i.e., IL10 and IL1RN, increase within 6 h [60,74]. The inflammation is usually cleared within 48-72 h [3,10].…”

“…Susceptibility of a mares to persisting endometritis is characterized by a failure to resolve (experimental) bacterial or breeding-induced endometritis within 72 h [3,59,74]. The reported incidence in broodmares is about 15% [74], and an older age and endometrosis represent predisposing factors [74].…”

“…Susceptibility of a mares to persisting endometritis is characterized by a failure to resolve (experimental) bacterial or breeding-induced endometritis within 72 h [3,59,74]. The reported incidence in broodmares is about 15% [74], and an older age and endometrosis represent predisposing factors [74]. Other associated factors are anatomical abnormalities of uterus and cervix [12], an increased angle of declination of the vulva [12], impaired myometrial contractions [11,74], and a dysregulation of inflammatory and immune mechanisms [12,59,60,74,79].…”