
Activation of NADPH oxidase is essential, but not sufficient, in controlling intracellular multiplication of B urkholderia pseudomallei in primary human monocytes
Author(s) -
Wikraiphat Chanthiwa,
Pudla Matsayapan,
Baral Pankaj,
Kitthawee Sangvorn,
Utaisincharoen Pongsak
Publication year - 2014
Publication title -
pathogens and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.983
H-Index - 105
ISSN - 2049-632X
DOI - 10.1111/2049-632x.12122
Subject(s) - burkholderia pseudomallei , nadph oxidase , intracellular , apocynin , intracellular parasite , microbiology and biotechnology , biology , melioidosis , oxidase test , reactive oxygen species , biochemistry , bacteria , enzyme , genetics
B urkholderia pseudomallei is a G ram‐negative intracellular bacterium and the causative agent of melioidosis. Innate immune mechanisms against this pathogen, which might contribute to outcomes of melioidosis, are little known. We demonstrated here that B . pseudomallei could activate NADPH oxidase in primary human monocytes as judged by production of reactive oxygen species ( ROS ) and p40 phox phosphorylation after infection. However, as similar to other intracellular bacteria, this bacterium was able to resist and multiply inside monocytes despite being able to activate NADPH oxidase. In the presence of NADPH oxidase inhibitor, diphenyleneiodonium or apocynin, intracellular multiplication of B . pseudomallei was significantly increased, suggesting that NADPH oxidase‐mediated ROS production is essential in suppressing intracellular multiplication of B . pseudomallei . Additionally, interferon‐γ ( IFN ‐γ)‐mediated intracellular killing of B . pseudomallei requires NADPH oxidase activity, even though ROS level was not detected at higher levels in IFN ‐γ‐treated infected monocytes. Altogether, these results imply that the activation of NADPH plays an essential role in suppressing intracellular multiplication of B . pseudomallei in human monocytes, although this enzyme is not sufficient to stop intracellular multiplication.