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- Transcription level analysis of intracellular Burkholderia pseudomallei illustrates the role of BPSL1502 during bacterial interaction with human lung epithelial cells
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Teerasit Techawiwattanaboon , Tanachaporn Bartpho , Rasana Wongratanacheewin Sermswan , Sorujsiri Chareonsudjai
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J. Microbiol. 2015;53(2):134-140. Published online January 28, 2015
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DOI: https://doi.org/10.1007/s12275-015-4522-9
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Abstract
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Melioidosis caused by Burkholderia pseudomallei is a globally
important disease of increasing concern according to high
case
-fatality rate and epidemic spreading. The ability of B.
pseudomallei to attach and invade host cells and subsequently
survive intracellularly has stimulated many questions concerning
the comprehension of bacterial pathogenesis progression.
Transcription levels of intracellular B. pseudomallei
genes in human lung epithelial cells were therefore analyzed
using bioinformatic tools, RT-PCR and real time RT-PCR.
Here, it is reported that the identification of bpsl1502, encoding
B. pseudomallei SurE (stationary phase survival protein
E) located in a global transcriptional regulation operon was
accomplished. The up-regulation of B. pseudomallei SurE was
demonstrated during intracellular survival of A549 cells at
12, 18, and 24 h post-infection. To investigate the role of
this protein, a B. pseudomallei SurE defective mutant was
constructed. The invasion and initial survival of the SurE
mutants within the A549 cells were impaired. There was no
difference, however, between the growth of B. pseudomallei
SurE mutant as compared to the wild type in Luria-Bertani
culture. These data suggest that SurE may assist B. pseudomallei
host cells invade and facilitate early intracellular infection
but is not crucial during the stationary growth phase.
The identification of B. pseudomallei SurE provides more
information of bacterial strategy during an early step of the
pathogenesis process of melioidosis.
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Citations
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PLOS ONE.2016; 11(8): e0160741. CrossRef - A predicted cation transporter protein, BPSS1228, is involved in intracellular behaviour ofBurkholderia pseudomalleiin a human lung epithelial cell line (A549)
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PLOS ONE.2016; 11(11): e0167355. CrossRef - Mechanisms of Disease: Host-Pathogen Interactions between Burkholderia Species and Lung Epithelial Cells
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Frontiers in Cellular and Infection Microbiology.2015;[Epub] CrossRef
- Role of a Burkholderia pseudomallei Polyphosphate Kinase in an Oxidative Stress Response, Motilities, and Biofilm Formation
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Suda Tunpiboonsak , Rungrawee Mongkolrob , Kaniskul Kitudomsub , Phawatwaristh Thanwatanaying , Witcha Kiettipirodom , Yanin Tungboontina , Sumalee Tungpradabkul
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J. Microbiol. 2010;48(1):63-70. Published online March 11, 2010
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DOI: https://doi.org/10.1007/s12275-010-9138-5
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Scopus
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Abstract
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Burkholderia pseudomallei, a motile and rod Gram-negative bacterium, is the causative agent of melioidosis. The bacterium is an intracellular pathogen and that motility is generally crucial for their survival in a natural environment and for systemic infection inside a host. We report here a role of B. pseudomallei polyphosphate kinase in virulence, such as an oxidative stress response, motilities and biofilm formation. The polyphosphate kinase (ppk) mutant is susceptible to hydrogen peroxide in an oxidative stress condition, unable to perform swimming, swarming motilities, and has lower density biofilm forming capacity than the wild-type strain. We also demonstrated that both polyphosphate kinase and motile flagella are essential and independently involved in biofilm formation. The B. pseudomallei flagellin (fliC) mutant and B. mallei, a nonmotile species, are shown to produce higher density biofilm formation than the ppk mutant, but less than wild type B. pseudomallei.