Publication: Burkholderia pseudomallei-Induced expression of a negative regulator, sterile-α and Armadillo motif-containing protein, in mouse macrophages: A possible mechanism for suppression of the MyD88-independent pathway
Issued Date
2011-07-01
Resource Type
ISSN
10985522
00199567
00199567
Other identifier(s)
2-s2.0-79959424118
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Infection and Immunity. Vol.79, No.7 (2011), 2921-2927
Suggested Citation
M. Pudla, K. Limposuwan, P. Utaisincharoen Burkholderia pseudomallei-Induced expression of a negative regulator, sterile-α and Armadillo motif-containing protein, in mouse macrophages: A possible mechanism for suppression of the MyD88-independent pathway. Infection and Immunity. Vol.79, No.7 (2011), 2921-2927. doi:10.1128/IAI.01254-10 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/12027
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Burkholderia pseudomallei-Induced expression of a negative regulator, sterile-α and Armadillo motif-containing protein, in mouse macrophages: A possible mechanism for suppression of the MyD88-independent pathway
Author(s)
Other Contributor(s)
Abstract
Burkholderia pseudomallei, a causative agent of melioidosis, is a Gram-negative facultative intracellular bacterium that can survive and multiply in macrophages. Previously, we demonstrated that B. pseudomallei failed to activate gene expression downstream of the MyD88-independent pathway, particularly the expression of beta interferon (IFN-β) and inducible nitric oxide synthase (iNOS), leading to the inability of macrophages to kill this bacterium. In the present report, we extended our study to show that B. pseudomallei was able to activate sterile-β and Armadillo motif (SARM)-containing protein, a known negative regulator of the MyD88-independent pathway. Both live B. pseudomallei and heat-killed B. pseudomallei were able to upregulate SARM expression in a time-dependent manner in mouse macrophage cell line RAW 264.7. The expression of SARM required bacterial internalization, as it could be inhibited by cytochalasin D. In addition, the intracellular survival of B. pseudomallei was suppressed in SARM-deficient macrophages. Increased expression of IFN-β and iNOS and degradation of I K Bα correlated with enhanced macrophage killing capability. These results demonstrated that B. pseudomallei modulated macrophage defense mechanisms by upregulating SARM, thus leading to the suppression of IFN-β and iNOS needed for bacterial elimination. © 2011, American Society for Microbiology.