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来自克罗恩氏病患者的便余物诱导M2巨细胞和纤维细胞的炎症变化
Frida Gorreja1, Mia Bendix2, Stephen T A Rush1
1Department of Microbiology and Immunology, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, 405 30 Gothenburg, Sweden.
来自克罗恩病 (CD) 患者的便超改变了肠道巨细胞和纤维细胞的反应,促进了炎症,但不是纤维化. 肠道微生物群代谢物在CD炎症中起着关键作用.
科学领域:
- 胃肠道学和免疫学
- 微生物组研究 微生物组研究
- 细胞生物学 细胞生物学
背景情况:
- 肠道巨细胞和纤维细胞是克罗恩病 (CD) 发病过程中的关键参与者.
- 肠道微生物组及其代谢物显著影响肠道微环境.
研究的目的:
- 研究CD患者的便超物 (FSs) 对巨细胞和纤维细胞行为的影响.
- 了解CD相关的便代谢物如何影响与炎症和纤维化相关的细胞功能.
主要方法:
- 从CD患者和健康受试者 (HS) 中收集了便超沉积物 (FS).
- 分析了FSs的代谢物概况.
- 由单细胞衍生的M2巨细胞和纤维细胞用FSs进行了培养.
- 分析包括分泌和表面蛋白质,基因表达和巨细胞体.
主要成果:
- 与HS-FS相比,CD-FS呈现出明显的代谢物概况.
- 在M2巨细胞中,CD-FS诱导了一种抗炎性表型 (增加IL-10,IL1RA,CD206),但没有改变效细胞化.
- 在纤维细胞中,CD-FS增加了亲炎性介质 (IL-6,MCP-1),但没有影响细胞外基质的产生.
- 巨受条件介质暴露于CD-FS调节的纤维细胞基因表达,影响TGFβ超级家族成员并减少IL-4.
结论:
- M2巨细胞和纤维细胞对CD便微环境表现出异常反应.
- 改变的蛋白质表达表明在CD中炎症延续起作用,而不是纤维化.
- 肠道微生物群的代谢物与克罗恩病的炎症的发展和/或维持有关.
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