聚合物免疫球蛋白受体将肺炎球菌转移到人类鼻上皮细胞中
J R Zhang1, K E Mostov, M E Lamm
1Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Cell
|October 13, 2000
概括
人类聚合物免疫球蛋白受体 (hpIgR) 与肺炎球菌CbpA结合,增强细菌的粘附和入侵. 这种相互作用凸显了病原体如何利用宿主粘膜免疫机制感染.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 细胞生物学 细胞生物学
背景情况:
- 聚合物免疫球蛋白受体 (pIgR) 对粘膜免疫至关重要,通过表皮屏障传输聚合物免疫球蛋白 (pIg).
- 微生物病原体经常利用宿主细胞机械来促进感染和殖民.
研究的目的:
- 为了研究人类聚合物免疫球蛋白受体 (hpIgR) 和肺炎 estreptococcus之间的相互作用.
- 确定 hpIgR 是否促进肺炎球菌通过粘膜表面的粘附和侵入.
主要方法:
- 同免疫沉试验评估hpIgR与肺炎球菌粘合素CbpA之间的结合.
- 使用人类鼻细胞和表达hpIgR的MDCK细胞进行细胞培养实验.
- 评估肺炎球菌粘附和入侵在存在或缺乏hpIgR,CbpA和特定抗体的情况下.
主要成果:
- 人类pIgR (hpIgR) 直接与肺炎球菌粘合素CbpA结合.
- 在细胞模型中,hpIgR的表达显著增强了肺炎球菌的附着性和侵入性.
- 通过遗传淘汰或抗体破坏hpIgR-CbpA相互作用,消除了这种增强.
- 子pIgR (rpIgR) 不结合CbpA,也不增强肺炎球菌转位.
结论:
- 肺炎球菌利用CbpA粘附蛋白与hpIgR相互作用.
- 这种相互作用促进了肺炎球菌在粘膜上皮层的转移,代表了一种新的致病机制.
- 通过hpIgR介导的细胞转移是预防肺炎球菌感染的可向途径.
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