Matsayapan PudlaAnchasa KananurakKornkaew LimposuwanStitaya SirisinhaPongsak UtaisincharoenMahidol University2018-05-032018-05-032011-12-01Innate Immunity. Vol.17, No.6 (2011), 532-54017534267175342592-s2.0-83455206228https://repository.li.mahidol.ac.th/handle/20.500.14594/11412Burkholderia pseudomallei, a causative agent of melioidosis, is a facultative intracellular Gram-negative bacterium that can survive and multiply inside the macrophages. Toll-like receptors are one class of pattern recognition receptors (PRRs) that have been documented to play significant role in B. pseudomallei infection. In the present study, we investigated a potential role of nucleotide-binding oligomerization domain-containing protein 1 and 2 (NOD1 and NOD2), cytoplasmic pattern recognition receptors, in B. pseudomallei- infected mouse macrophage cell line RAW 264.7. Both live and heat-killed B. pseudomallei were able to up-regulate NOD1 and NOD2 expression in a time-dependent manner. Marked reduction of a negative regulator, suppressor of cytokine signaling 3 (SOCS3), expression was observed only in B. pseudomallei-infected NOD2-depleted macrophages and not in NOD1-depleted macrophages. The decrease in SOCS3 expression also led to an increase in IFN-γ responsiveness as judged by an enhanced STAT-1 phosphorylation on tyrosine 701 in the B. pseudomallei-infected macrophages. Together, these results suggested that, in addition to using other PRRs to evade macrophage defense, B. pseudomallei may also use NOD2 to regulate a negative regulator like SOCS3. © The Author(s) 2010 Reprints and permissions: sagepub.co.uk/ journalsPermissions.nav.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyImmunology and MicrobiologyMedicineArticleSCOPUS10.1177/1753425910385484