Defining postpartum uterine disease and the mechanisms of infection and immunity in the female reproductive tract in cattle.
Defining postpartum uterine disease and the mechanisms of infection and immunity in the female reproductive tract in cattle.
复制标题
DOI：
10.1095/biolreprod.109.077370
复制
发表时间：
2009-12
影响因子：
3.6
通讯作者：
Schuberth HJ
中科院分区：
文献类型：
--
作者：
Sheldon IM;Cronin J;Goetze L;Donofrio G;Schuberth HJ
子宫微生物病影响了一半的奶牛分娩后，通过破坏子宫和卵巢功能导致不孕。大肠杆菌、化脓性隐杆菌和牛疱疹病毒4型感染可引起子宫内膜组织损伤。子宫内膜细胞上的toll样受体（TLRs）检测病原体相关分子，如细菌DNA、脂质和脂多糖（LPS），导致细胞因子、趋化因子和抗微生物肽的分泌。趋化因子吸引中性粒细胞和巨噬细胞来消灭细菌，尽管中性粒细胞的持续存在与亚临床子宫内膜炎和不孕症有关。子宫感染的奶牛不太可能排卵，因为它们产后卵巢优势卵泡生长较慢，外周血浆雌二醇浓度较低，下丘脑和垂体功能紊乱。子宫内膜炎动物的卵泡液中含有LPS，通过颗粒细胞上的TLR4/CD14/LY96 （MD2）受体复合物检测到LPS，导致芳香化酶表达降低，雌二醇分泌减少。患有子宫疾病的奶牛排卵时，外周血血浆黄体酮浓度低于正常动物。然而，在患有子宫疾病的动物中，黄体期经常延长，这可能是因为感染通过磷脂酶A2介导的机制将子宫内膜上皮前列腺素的分泌从F系列切换到E系列，这将破坏黄体溶解。子宫内膜免疫的调节依赖于类固醇激素、生长激素和局部调节蛋白。应利用对女性生殖道感染和免疫知识的新进展来开发子宫疾病的新疗法。
Uterine microbial disease affects half of all dairy cattle after parturition, causing infertility by disrupting uterine and ovarian function. Infection with Escherichia coli, Arcanobacterium pyogenes and bovine herpesvirus 4 causes endometrial tissue damage. Toll-like receptors (TLRs) on endometrial cells detect pathogen-associated molecules such as bacterial DNA, lipids and lipopolysaccharide (LPS), leading to secretion of cytokines, chemokines and anti-microbial peptides. Chemokines attract neutrophils and macrophages to eliminate the bacteria, although persistence of neutrophils is associated with subclinical endometritis and infertility. Cows with uterine infections are less likely to ovulate because they have slower growth of the postpartum dominant follicle in the ovary, lower peripheral plasma estradiol concentrations, and perturbation of hypothalamic and pituitary function. The follicular fluid of animals with endometritis contains LPS, which is detected by the TLR4/CD14/LY96 (MD2) receptor complex on granulosa cells leading to lower aromatase expression and reduced estradiol secretion. If cows with uterine disease ovulate, the peripheral plasma concentrations of progesterone are lower than in normal animals. However luteal phases are often extended in animals with uterine disease, probably because infection switches the endometrial epithelial secretion of prostaglandins from the F to the E series, by a phospholipase A2 mediated mechanism, which would disrupt luteolysis. The regulation of endometrial immunity depends on steroid hormones, somatotrophins and local regulatory proteins. Advances in knowledge about infection and immunity in the female genital tract should be exploited to develop new therapeutics for uterine disease.
登录
查看更多内容
DOI：
10.1530/rep-08-0171
发表时间：
2008-09
期刊：
Reproduction (Cambridge, England)
影响因子：
--
作者：
Donofrio G;Ravanetti L;Cavirani S;Herath S;Capocefalo A;Sheldon IM
通讯作者：
Sheldon IM
影响因子：
3.6
作者：
Beam, SW;Butler, WR
通讯作者：
Butler, WR
影响因子：
2.8
作者：
GRIFFIN J F T;HARTIGAN P J;NUNN W R
通讯作者：
NUNN W R
影响因子：
4.4
作者：
Davies, Darren;Meade, Kieran G.;Sheldon, I. Martin
通讯作者：
Sheldon, I. Martin
影响因子：
3.3
作者：
Hansen, P. J.
通讯作者：
Hansen, P. J.