脂多糖体内毒素会触发炎症反应,破坏颗粒细胞的功能,改变细胞生长动态
Briza Castro1, Jeffrey F Dominguez Arellanes1, Charles B Shuster2
1Department of Animal and Range Sciences, New Mexico State University, Las Cruces, NM 88003, United States.
Reproductive toxicology (Elmsford, N.Y.)
|November 20, 2025
概括
低水平的内毒素脂多聚糖化物 (LPS) 暴露会增加人类颗粒细胞中的促炎性细胞因子. 较高的LPS度会降低细胞增殖,但卵泡刺激激素 (FSH) 可能会提供对LPS诱导的卵巢功能障碍的保护.
科学领域:
- 生殖生物学 生殖生物学
- 内分泌学 在内分泌学.
- 免疫学 免疫学 免疫学
背景情况:
- 格拉姆阴性细菌内毒素脂聚糖 (LPS) 通过损害颗粒细胞功能和生育能力来破坏雌性生殖.
- 从亚临床感染中低水平的LPS暴露对生殖健康的影响尚不清楚.
研究的目的:
- 为了研究增加LPS度对人体颗粒状细胞 (KGN) 细胞生长,免疫反应和类固醇生成的影响.
- 为了确定毛囊刺激激素 (FSH) 是否调节LPS对KGN细胞的影响.
主要方法:
- 在48小时内,KGN细胞在不同的LPS度 (0.0001-10μg/mL) ±FSH下进行培养.
- 用实时成像评估细胞增殖.
- 量化了类固醇和炎症标记物的基因表达 (STAR,CTNNB1,CYP19A,IL-6,IL-8,MCP-1,NF-κB).
- 孕激素和雌激素水平在培养基中测量.
主要成果:
- 在1和10μg/mL的度下,LPS剂量依赖增加了促炎性细胞因子表达 (IL-6,IL-8,MCP-1).
- 较高的LPS度 (1和10微克/毫升) 降低了KGN细胞汇合 (增殖).
- 仅FSH治疗就降低了CTNNB1和增加了CYP19A的表达,但对于类固醇基因,没有观察到显著的LPS × FSH相互作用.
- LPS增加了STAR mRNA的丰度,特别是在10μg/mL时,但没有影响孕激素或雌激素水平.
结论:
- 低剂量的LPS暴露会触发颗粒状细胞中的炎症反应.
- 高度的LPS抑制了花质细胞的增殖,这种效应可能被FSH减轻.
- FSH可能提供对LPS诱导的卵巢功能障碍的保护作用,这需要进一步调查.
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