Jaruek CharoensapAnneke EngeringPongsak UtaisincharoenYvette van KooykStitaya SirisinhaMahidol UniversityVU University Medical Center2018-07-122018-07-122008-12-01Transactions of the Royal Society of Tropical Medicine and Hygiene. Vol.102, No.SUPPL. 1 (2008)003592032-s2.0-58049157336https://repository.li.mahidol.ac.th/handle/20.500.14594/19258Summary: Dendritic cells (DCs) are essential in regulating adaptive immunity. DC-SIGN (DC-specific ICAM-grabbing nonintegrin) is a C-type lectin receptor that is expressed mainly by DCs. Accumulating evidence supports that certain pathogens target DC-SIGN to escape host immunity. To investigate a possible role of DC-SIGN in Burkholderia pseudomallei infection, we initially screened its DC-SIGN binding activity by an ELISA method utilizing a DC-SIGN-Fc chimeric protein and found that all of the B. pseudomallei strains tested failed to bind DC-SIGN. However, one strain, the LPS mutant SRM117, which lacks the type II O-polysaccharide expression, actually bound DC-SIGN, in contrast to its wild-type counterpart 1026b (P < 0.001). We also found that, although the LPS mutant could readily activate monocyte-derived human DCs, it induced lower levels of IL-12p70 and IL-10 production than its wild-type counterpart (P < 0.01). By contrast, the wild-type and the LPS mutants were indistinguishable from one another in terms of TH1/TH2 differentiation. Altogether, these data suggest that, unlike other certain host pathogen interactions, activation of DCs by B. pseudomallei is not dependent on DC-SIGN. We also found evidence that the LPS mutant that binds DC-SIGN has a suppressive effect on DC cytokine production. © 2008 Elsevier Ltd. All rights reserved.Mahidol UniversityImmunology and MicrobiologyMedicineArticleSCOPUS10.1016/S0035-9203(08)70020-8