Bozhokina E S, Kever L V, Komissarchik Ya Yu, Khaitlina S Yu, Efremova T N
Tsitologiia. 2015;57(10):714-9.
Facultative pathogens Serratia grimesii are able to invade eukaryotic cells where they have been found in vacuoles and free in the cytoplasm (Efremova et al., 2001; Bozhokina et al., 2011). However, efficiency of this invasion is low, and the mechanisms of the invasion related to the initial steps of the process are not known. In the present study, we have increased the invasion efficiency by incubation of HeLa cells with N-acetylcysteine (NAC) preceding the infection. In the NAC-pretreated cells, two modes of S. grimesii to enter HeLa cells were observed. In the most cases, the penetration of S. grimesii into the cell was consistent with the "zipper mechanism", involving specific interaction of bacterial invasin with a host cell surface receptor. However, in some cases, bacteria were trapped by membrane ruffling probably produced by injected bacterial proteins that trigger the bacterial uptake process, as described in the "trigger mechanism". Further elucidation of bacterial and cellular factors involved in the bacteria-host cell interaction should clarify whether two different mechanisms or a predominant one operate during S. grimesii invasion.
兼性病原菌格氏沙雷氏菌能够侵入真核细胞,在液泡中以及细胞质中均发现过它们的踪迹(叶夫列莫娃等人,2001年;博若基娜等人,2011年)。然而,这种侵入的效率很低,且与该过程初始步骤相关的侵入机制尚不清楚。在本研究中,我们通过在感染前用N - 乙酰半胱氨酸(NAC)孵育HeLa细胞提高了侵入效率。在经NAC预处理的细胞中,观察到格氏沙雷氏菌进入HeLa细胞的两种模式。在大多数情况下,格氏沙雷氏菌进入细胞的过程与“拉链机制”一致,涉及细菌侵袭素与宿主细胞表面受体的特异性相互作用。然而,在某些情况下,细菌被可能由注入的细菌蛋白产生的膜皱褶捕获,从而引发细菌摄取过程,这与“触发机制”中所描述的情况相同。对参与细菌与宿主细胞相互作用的细菌和细胞因子的进一步阐明,应能明确在格氏沙雷氏菌侵入过程中是两种不同机制起作用,还是一种主要机制起作用。