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International Journal of Microbiology
Volume 2012 (2012), Article ID 917031, 8 pages
Research Article

Temperature Depended Role of Shigella flexneri Invasion Plasmid on the Interaction with Acanthamoeba castellanii

Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute and Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden

Received 28 August 2011; Revised 24 November 2011; Accepted 9 December 2011

Academic Editor: Jianwu Pei

Copyright © 2012 Amir Saeed et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Shigella flexneri is a Gram-negative bacterium causing the diarrhoeal disease shigellosis in humans. The virulence genes required for invasion are clustered on a large 220 kb plasmid encoding type three secretion system (TTSS) apparatus and virulence factors such as adhesions and invasion plasmid antigens (Ipa). The bacterium is transmitted by contaminated food, water, or from person to person. Acanthamoebae are free-living amoebae (FLA) which are found in diverse environments and isolated from various water sources. Different bacteria interact differently with FLA since Francisella tularensis, Vibrio cholerae, Shigella sonnei, and S. dysenteriae are able to grow inside A. castellanii. In contrast, Pseudomonas aeruginosa induces both necrosis and apoptosis to kill A. castellanii. The aim of this study is to examine the role of invasion plasmid of S. flexneri on the interaction with A. castellanii at two different temperatures. A. castellanii in the absence or presence of wild type, IpaB mutant, or plasmid-cured strain S. flexneri was cultured at C and C and the interaction was analysed by viable count of both bacteria and amoebae, electron microscopy, flow cytometry, and statistical analysis. The outcome of the interaction was depended on the temperature since the growth of A. castellanii was inhibited at C, and A. castellanii was killed by invasion plasmid mediated necrosis at C.