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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/42978
Title: Burkholderia pseudomallei rpoS mediates iNOS suppression in human hepatocyte (HC04) cells
Authors: Sucharat Sanongkiet
Saranyoo Ponnikorn
Rachanee Udomsangpetch
Sumalee Tungpradabkul
Mahidol University
Thammasat University
Keywords: Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology
Issue Date: 1-Aug-2016
Citation: FEMS Microbiology Letters. Vol.363, No.15 (2016)
Abstract: © FEMS 2016. Burkholderia pseudomallei is an intracellular Gram-negative bacterial pathogen and the causative agent of melioidosis, a widespread disease in Southeast Asia. Reactive nitrogen, in an intermediate form of nitric oxide (NO), is one of the first lines of defense used by host cells to eliminate intracellular pathogens, through the stimulation of inducible nitric oxide synthase (iNOS). Studies in phagocytotic cells have shown that the iNOS response is muted in B. pseudomallei infection, and implicated the rpoS sigma factor as a key regulatory factor mediating suppression. The liver is a main visceral organ affected by B. pseudomallei, and there is little knowledge about the interaction of liver cells and B. pseudomallei. This study investigated the induction of iNOS, as well as autophagic flux and light-chain 3 (LC3) localization in human liver (HC04) cells in response to infection with B. pseudomallei and its rpoS deficient mutant. Results showed that the rpoS mutant was unable to suppress iNOS induction and that the mutant showed less induction of autophagy and lower co-localization with LC3, and this was coupled with a lower intracellular growth rate. Combining these results suggest that B. pseudomallei rpoS is an important factor in establishing infection in liver cells.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84982921052&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/42978
ISSN: 15746968
03781097
Appears in Collections:Scopus 2016-2017

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