ENTRY OF FACULTATIVE PATHOGEN SERRATIA GRIMESII INTO HELA CELLS.
ELECTRON MICROSCOPIC ANALYSIS
E.S. Bozhokina, L.V. Kever, Ya Yu. Komissarchik, S.Yu. Khaitlina,1 T.N. Efremova
Institute of Cytology RAS, St. Petersburg, 194064;
1 e-mail: skhspb@gmail.com
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 mecha-nism", 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.
Key words:
bacterial invasion, N-acetylcysteine, Serratia grimesii, invasion steps
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