Panthong KulsantiwongMatsayapan PudlaJitrada BoonditChanthiwa WikraiphatSusanna J. DunachieNarisara ChantratitaPongsak UtaisincharoenMahidol University2018-12-112019-03-142018-12-112019-03-142016-06-01Medical Microbiology and Immunology. Vol.205, No.3 (2016), 255-26014321831030085842-s2.0-84946887898https://repository.li.mahidol.ac.th/handle/123456789/40812© 2015, Springer-Verlag Berlin Heidelberg. Burkholderia pseudomallei, a gram-negative intracellular bacterium, is a causative agent of melioidosis. The bacterium has been shown to induce the innate immune response, particularly pro-inflammatory cytokine production in several of both mouse and human cell types. In the present study, we investigate host immune response in B. pseudomallei-infected primary human monocytes. We discover that wild-type B. pseudomallei is able to survive and multiply inside the primary human monocytes. In contrast, B. pseudomallei LPS mutant, a less virulent strain, is susceptible to host killing during bacterial infection. Moreover, microarray result showed that wild-type B. pseudomallei but not B. pseudomallei LPS mutant is able to activate gene expression of IL-23 as demonstrated by the up-regulation of p19 and p40 subunit expression. Consistent with gene expression analysis, the secretion of IL-23 analyzed by ELISA also showed that wild-type B. pseudomallei induces a significantly higher level of IL-23 secretion than that of B. pseudomallei LPS mutant. These results implied that IL-23 may be an important cytokine for the innate immune response during B. pseudomallei infection. The regulation of IL-23 production may drive the different host innate immune responses between patients and may relate to the severity of melioidosis.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1007/s00430-015-0440-z