Lipopolysaccharide-induced mechanisms of ovarian dysfunction in cows with uterine inflammatory diseases
Lipopolysaccharide-induced mechanisms of ovarian dysfunction in cows with uterine inflammatory diseases
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DOI：
10.1262/jrd.2020-021
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发表时间：
2020-08-01
影响因子：
1.8
通讯作者：
Magata, Fumie
中科院分区：
文献类型：
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作者：
Magata, Fumie
子宫炎性疾病通常发生在产后奶牛中，由于子宫和卵巢活动异常导致繁殖性能降低。子宫感染革兰氏阴性菌导致奶牛血浆和卵泡液中检测到脂多糖（LPS）沿着子宫炎症。LPS作用于卵泡成分，如卵泡膜细胞、颗粒细胞和卵泡封闭的卵母细胞，导致卵泡活性受损。由于类固醇生成酶转录的抑制，高LPS环境下的卵泡表现出卵泡类固醇生成减少。牛颗粒细胞和卵泡膜细胞的原代细胞培养物已经表明，LPS作用于卵泡细胞以损害类固醇产生，这可能干扰卵泡生长和/或降低其排卵能力。即使发生排卵，患有子宫炎症的奶牛也不太可能怀孕，因为除了子宫损伤外，LPS还损害卵母细胞的发育能力。LPS干扰牛卵母细胞的核质成熟。此外，使用LPS处理成熟的卵母细胞不太可能发育到胚泡阶段。这样的卵母细胞在胚泡中也具有减少的滋养层细胞数量。因此，LPS对卵巢活性的不利影响可能是子宫炎症奶牛不孕的部分原因。子宫炎性疾病的新的治疗和预防策略可以通过提高我们对卵巢功能障碍的病理生理学的认识来开发，这只能通过进一步的研究来实现。本文综述了脂多糖诱导卵巢功能障碍的分子发病机制。
Uterine inflammatory diseases commonly occur in postpartum dairy cows, resulting in reduced reproductive performance due to aberrant uterine and ovarian activity. Infection of the uterus with gram-negative bacteria results in the detection of lipopolysaccharide (LPS) in the plasma and follicular fluid of cows along with uterine inflammation. LPS acts on follicular components such as theca cells, granulosa cells, and follicle-enclosed oocytes, leading to impaired follicular activity. Follicles with a high LPS environment exhibit reduced follicular steroidogenesis due to the inhibition of steroidogenic enzyme transcription. Primary cell cultures of bovine granulosa and theca cells have shown that LPS acts on follicular cells to impair steroid production, which may disturb follicle growth and/or reduce their ability to ovulate. Even if ovulation occurs, cows with uterine inflammation are less likely to conceive because in addition to uterine damage, LPS also impairs the developmental competence of oocytes. LPS perturbs the nuclear and cytoplasmic maturation of bovine oocytes. Moreover, oocytes matured using LPS treatment are less likely to develop into the blastocyst stage. Such oocytes also have a reduced number of trophoblast cells in blastocysts. Therefore, the detrimental effects of LPS on ovarian activity may be partly responsible for infertility in cows with uterine inflammation. Novel treatment and prevention strategies for uterine inflammatory diseases can be developed by advancing our knowledge of the pathophysiology underlying ovarian dysfunction, and this can only be achieved by further research. The present review outlines the molecular pathogenesis of LPS-induced ovarian dysfunction.