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在Physioxia下的MCT依赖的Cryptosporidium parvum诱导的牛单细胞细胞外陷 (METs)
Seyed Sajjad Hasheminasab1, Iván Conejeros1, Ulrich Gärtner2
1Institute of Parasitology, Biomedical Research Center Seltersberg (BFS), Justus Liebig University Giessen, 35392 Giessen, Germany.
Biology
|July 29, 2023
概括
单细胞细胞外陷 (METs) 通过捕获卵囊和阻碍杂虫细胞来对抗Cryptosporidium parvum. 在低氧条件下,这种防御依赖乳酸单碳酸盐输送体 (MCT),而不是P2X1依赖.
科学领域:
- 免疫学 免疫学 免疫学
- 寄生虫学的寄生虫学
- 细胞生物学 细胞生物学
背景情况:
- Cryptosporidium parvum会在人类和动物中引起动物性菌性菌病.
- 单细胞是具有抗寄生虫功能的关键先天性免疫细胞.
- 单细胞细胞外陷 (METs) 是一种新兴的对抗寄生虫的防御机制.
研究的目的:
- 调查ATP纯能受体P2X1,糖解,诺奇信号传导和乳酸单碳酸盐运输体 (MCT) 在Cryptosporidium parvum诱导的牛单细胞中MET形成中的作用.
- 为了确定在肠道物理和高氧下METosis的依赖氧的性质.
- 阐明METs在对抗C. parvum卵和杂虫的机制.
主要方法:
- 在不同氧气条件下 (5% O2和21% O2) 暴露牛单细胞于C. parvum.
- 使用P2X1抗剂 (NF449),糖解抑制剂 (2-DG),MCT抑制剂 (AR-C 141990) 和Notch抑制剂 (DAPT,化合物E) 的抑制研究.
- 显微镜技术包括免疫光,共聚焦,扫描电子显微镜 (SEM) 和活细胞3D全息显微镜.
- 测量单细胞能量状态 (ECAR和OCR).
主要成果:
- 证实了由C. parvum诱导的自杀性MET,导致卵囊被困,并阻碍了杂虫细胞的运动.
- MET形成是P2X1独立的,并且仅部分依赖于糖解.
- 在物理氧化条件下 (5% O2) ,MCT抑制显著降低了MET挤出.
- 标记信号抑制没有影响牛的市场营销待遇生产.
- 单细胞在暴露于C. parvum时没有改变ECAR或OCR.
结论:
- C. parvum介导的METosis是一种独立于P2X1但依赖于MCT的防御机制.
- METs通过捕捉寄生虫和抑制杂虫菌的存在,有助于产生抗密码体效应.
- 这项研究强调了MCT在肠道物理中对C. parvum的单细胞介导免疫力中的重要性.
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