肺炎链球菌表面蛋白在细菌体外粘附中的介导作用

The mediatory effects of pneumococcal surface proteins on the adherence of bacteria to host cell in vitro

目的在体外研究肺炎链球菌表面蛋白对细菌粘附于宿主细胞的介导作用。方法用ＦＩＴＣ荧光标记肺炎链球菌（ＳⅡ、ＳⅢ），用蛋白质合成抑制剂，ＲＮＡ合成抑制剂和神经氨酸酶分别处理肺炎链球菌和小鼠腹腔巨噬细胞后，在体外观察这些因素对细菌与巨噬细胞粘附率的影响；另外观察细菌细胞壁提取物对上述粘附率的影响。结果证实了粘附过程存在剂量依赖和时间依赖的关系，是特异的粘附过程。用多因素分别处理肺炎链球菌和巨噬细胞后，其粘附率的改变与肺炎链球菌合成ＲＮＡ和蛋白质有关，需要肺炎链球菌识别巨噬细胞表面糖蛋白结构的受体。肺炎链球菌可溶性细胞壁成分能与完整肺炎链球菌同样有对巨噬细胞的粘附，去蛋白细胞壁成分则无此作用。结论提示细菌表面蛋白介导了这一粘附过程。

Objective The Gram positive bacterium Streptococcus pneumoniae is a major pathogen of pneumonia,sepsis and meningitis. To gain access to tissue within the human host, Streptococcus pnumoniae must initially attach to the surface of host cell. The recent research reported that the cell wall could mediate Streptococcus pneumoniae attachment to human endothelial cells. Although the factors of pneumococcal adhesions are still currently unknown,the surface proteins of S. pneumoniae are thought to be the potential candidates. Methods In this study, S. pneumoniae (SⅡ,SⅢ) were labelled by FITC, then the bacteria and mice macrophages were pretreated with the RNA,protein synthetic inhibitors and purified pneumococcal cell wall components,respectively. The effects on the adherence between the bacteria and macrophages were studied. Results The adherence of S.pneumoniae to macrophages was in a dose and time dependent fashion, suggesting that the interaction is specific. S.pneumoniae and macrophages were pretreated with various factors,respectively,then the adherece results of S. pneumoniae to macrophages indicated that the active bacterial protein and RNA synthesis were essential for adherence of S. pneumoniae to macrophages,The recognization between S. pneumoniae and surface receptors with glycoproteins of macrophages is essential, The soluble pneumococcal cell wall components decreased the ability of adherence of intact S.pneumoniae to the macrophages in a dose dependent fashion, However,non protein cell wall molecules were inactive. Conclusions These results suggest that pneumococcal cell wall proteins mediate the interaction.