title: [ENTRY OF FACULTATIVE PATHOGEN SERRATIA GRIMESII INTO HELA CELLS. ELECTRON MICROSCOPIC ANALYSIS].
abstract: 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.
authors: E S
authors: ES
authors: Bozhokina
authors: L V
authors: LV
authors: Kever
authors: Ya Yu
authors: YY
authors: Komissarchik
authors: S Yu
authors: SY
authors: Khaitlina
authors: T N
authors: TN
authors: Efremova
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D018829:Adhesins, Bacterial / Q000378:metabolism; D003593:Cytoplasm / Q000187:drug effects / Q000648:ultrastructure*; D005057:Eukaryotic Cells / Q000187:drug effects / Q000648:ultrastructure*; D006367:HeLa Cells; D054884:Host-Pathogen Interactions; D006801:Humans; D008854:Microscopy, Electron; D012705:Serratia / Q000378:metabolism / Q000472:pathogenicity / Q000648:ultrastructure*
chemical_list: D018829:Adhesins, Bacterial; D000111:Acetylcysteine