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Total Protein Extraction and 2-D Gel Electrophoresis Methods for Burkholderia Species
Published on: October 15, 2013
Exploitation of host cells by Burkholderia pseudomallei
Mark P Stevens1, Edouard E Galyov
1Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire, United Kingdom.
Abstract:
Intracellular bacterial pathogens have evolved mechanisms to enter and exit eukaryotic cells using the power of actin polymerisation and to subvert the activity of cellular enzymes and signal transduction pathways. The proteins deployed by bacteria to subvert cellular processes often mimic eukaryotic proteins in their structure or function. Studies on the exploitation of host cells by the facultative intracellular pathogen Burkholderia pseudomallei are providing novel insights into the pathogenesis of melioidosis, a serious invasive disease of animals and humans that is endemic in tropical and subtropical areas. B. pseudomallei can invade epithelial cells, survive and proliferate inside phagocytes, escape from endocytic vesicles, form actin-based membrane protrusions and induce host cell fusion. Here we review current understanding of the molecular mechanisms underlying these processes.
Insights
Burkholderia pseudomallei invades host cells using actin polymerization to cause melioidosis. This review details the molecular strategies this pathogen uses to infect and spread within host cells.
Area of Science:
- Microbiology
- Cell Biology
- Pathogenesis
Background:
- Intracellular bacterial pathogens utilize host cell machinery for invasion and replication.
- Burkholderia pseudomallei is a facultative intracellular bacterium causing melioidosis, a significant human and animal disease.
- Understanding bacterial subversion of host processes is crucial for developing treatments.
Purpose of the Study:
- To review the molecular mechanisms by which Burkholderia pseudomallei exploits host cells.
- To provide insights into the pathogenesis of melioidosis.
Main Methods:
- Review of existing literature on Burkholderia pseudomallei pathogenesis.
- Analysis of bacterial strategies for host cell entry, survival, and exit.
- Examination of actin-based motility and host cell fusion mechanisms.
Main Results:
- B. pseudomallei invades epithelial cells and survives within phagocytes.
- The pathogen escapes endocytic vesicles and forms actin-based protrusions for cell-to-cell spread.
- B. pseudomallei induces host cell fusion, contributing to disease progression.
Conclusions:
- B. pseudomallei employs sophisticated molecular mechanisms to manipulate host cell functions.
- Understanding these mechanisms is key to combating melioidosis.
- Further research into bacterial protein mimicry of eukaryotic proteins may reveal therapeutic targets.
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