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Published on: May 21, 2018
Involvement of B. pseudomallei RpoS in apoptotic cell death in mouse macrophages
I Lengwehasatit1, A Nuchtas, S Tungpradabkul
1MU-OU:CRC and Department of Biotechnology, Faculty of Science, Mahidol University, Bangkok, Thailand. scilw@mahidol.ac.th
Abstract:
Burkholderia pseudomallei, the causative agent of melioidosis, is a facultative intracellular Gram-negative bacillus which can survive and multiply in both phagocytic and nonphagocytic cells. This bacterium could also induce apoptosis in various cell types. In the present study, we extend our finding to demonstrate the role of RpoS of B. pseudomallei in apoptosis induction. Unlike the wild-type strain, the B. pseudomallei rpoS mutant strain failed to induce cytotoxicity in mouse macrophages (RAW264.7). Furthermore, the mutant produced less extensive mitochondrial membrane potential changes and caspase-3 activation in the macrophages than did the wild-type strain. These data suggest that the RpoS of B. pseudomallei plays an essential role in the regulation of cell death in mouse macrophages.
Insights
The RpoS protein of Burkholderia pseudomallei is crucial for inducing cell death in mouse macrophages. A mutant lacking RpoS failed to cause cytotoxicity, indicating RpoS
Area of Science:
- Microbiology
- Cell Biology
- Immunology
Background:
- Burkholderia pseudomallei causes melioidosis and can survive within host cells.
- This bacterium is known to induce apoptosis in various cell types.
Purpose of the Study:
- To investigate the role of the RpoS protein in Burkholderia pseudomallei-induced apoptosis.
- To determine if RpoS is essential for the bacterium's cytotoxic effects on macrophages.
Main Methods:
- Comparison of wild-type B. pseudomallei and an rpoS mutant strain.
- Assessment of cytotoxicity in mouse macrophage cell lines (RAW264.7).
- Measurement of mitochondrial membrane potential and caspase-3 activation.
Main Results:
- The B. pseudomallei rpoS mutant strain showed significantly reduced cytotoxicity compared to the wild-type.
- The mutant induced less pronounced changes in mitochondrial membrane potential.
- Caspase-3 activation was lower in macrophages exposed to the rpoS mutant.
Conclusions:
- RpoS plays a critical role in Burkholderia pseudomallei's ability to induce apoptosis in mouse macrophages.
- The RpoS protein is essential for the bacterium's cytotoxic effects and regulation of cell death pathways.
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