通过激活胎儿-母亲界面上的标志物进行免疫调节,用于感染相关的自发早产
Tanu Bhati1, Ankita Ray1, Renu Arora2
1Molecular Microbiology Laboratory, ICMR-National Institute of Pathology, Sriramachari Bhawan, Safdarjung Hospital Campus, Post Box no. 4909, New Delhi 110029, India.
Cytokine
|August 18, 2023
概括
导致自发早产 (sPTB) 的感染会提高胎盘免疫激活标志物. CD66a,ICAM1和TIM3可能会促进早产,而CD25和CD95则表明感染期间的免疫耐受性.
科学领域:
- 免疫学 免疫学 免疫学
- 生殖生物学 生殖生物学
- 微生物学 微生物学
背景情况:
- 自发早产 (sPTB) 是一个重要的全球健康问题.
- 感染是sPTB的主要原因,涉及复杂的孕产妇免疫反应.
- 免疫激活标记物参与调节这些反应.
研究的目的:
- 为了研究免疫激活标记的mRNA表达 (CD66a,ICAM1,ITGB1,TIM3,CD25,CD95).
- 分析这些标记物与细胞因子 (IL-1β,IL-17) 和前列腺素受体 (EP2,IP) 的相关性.
- 为了检查由于Chlamydia trachomatis,Mycoplasma hominis和Ureaplasma urealyticum感染的sPTB妇女的胎盘中的这些因素.
主要方法:
- 从160名sPTB和160名产期妇女收集了胎盘样本.
- 使用PCR检测出了传染病原体 (C. trachomatis,M. hominis,U. urealyticum) 的存在.
- 实时qPCR被用于量化标记物,细胞因子和受体的mRNA表达.
主要成果:
- 在感染sPTB胎盘中观察到CD66a,ICAM1,TIM3,CD25和CD95的升调 (2.89至6.95倍) (p < 0.001).
- 细胞因子IL-1β和IL-17,以及前列腺素受体EP2和IP也显著上调 (4.71至5.5倍,p<0.001).
- 在ICAM-1和IL-1β/EP2/IL-17,TIM3和IP/IL-17之间发现了显著的相关性,以及CD66a,CD25和CD95与某些细胞因子/受体之间的反相关性.
结论:
- 在感染期间,CD66a,ICAM1和TIM3可能会导致炎症和早产.
- 尽管有感染,CD25和CD95可能参与维持胎儿-母亲免疫耐受性.
- 这些发现突出了sPTB风险和病原体的潜在生物标志物.
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