前列腺素E2的积累与S. aureus感染的牛子宫内膜炎密切相关
1School of Public Healthy, Inner Mongolia Medical University, 010110 Hohhot, China; Laboratory of Veterinary Pharmacology, College of Veterinary Medicine, Inner Mongolia Agricultural University, 010018 Hohhot, China.
Cytokine
|January 4, 2024
概括
前列腺素E2 (PGE2) 在由金黄色葡萄球菌引起的牛子宫内膜炎中起着关键作用. 减少PGE2积累有效地减轻活体和死体黄金色杆菌感染的炎症.
科学领域:
- 兽医免疫学 兽医免疫学
- 细菌病原体的产生
- 生殖免疫学 生殖免疫学
背景情况:
- 黄金葡萄球菌是牛子宫内膜炎的常见原因,经常被忽视为亚临床病原体.
- 之前的研究表明,活生生的金黄色细菌 (LSA) 和被热杀死的金黄色细菌 (HK-SA) 在牛子宫内引起了不同的炎症反应,可能与前列腺素E2 (PGE2) 积累有关.
研究的目的:
- 研究PGE2在HK-SA诱导的牛子宫内膜组织炎症中的作用.
- 探索牛子宫内膜上皮细胞 (BEC) 中的LSA,PGE2和炎症途径之间的关系.
- 确定S. aureus脂蛋白对PGE2生成和细胞反应的影响.
主要方法:
- 使用抑制剂/激动剂在接受HK-SA治疗的牛子宫内膜组织中的PGE2度变化.
- 用S. aureus菌株SA113及其脂蛋白淘汰突变体 (SA113Δlpl) 感染BEC.
- 测量炎症标志物 (IL-6,TNF-α,DAMPs),信号通路 (MAPK,PKA) 和细胞功能 (粘附,入侵).
主要成果:
- PGE2与IL-6,TNF-α,DAMPs (HMGB-1,HABP-1) 和组织损伤正相关,由EP4-p38 MAPK通路调节.
- 黄金色素脂蛋白与PGE2生成有关.
- 与SA113感染相比,LSA感染SA113Δlpl减少了PGE2,cAMP,EP4,IL-6,IL-8和MAPK/PKA信号传递.与SA113感染相比,LSA感染SA113Δlpl减少了PGE2,cAMP,EP4,IL-6,IL-8和MAPK/PKA信号传递.
- 脂蛋白淘汰也降低了BEC粘附和入侵的调节.
结论:
- PGE2是HK-SA和LSA诱导的牛子宫内膜炎症反应的组成部分.
- 黄金菌感染有助于牛子宫内膜炎.
- 准PGE2积累是一种潜在的治疗策略,可以减少S. aureus诱导的炎症,无论细菌活力如何.
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