Interaction of burkholderia pseudomallei with cells of the immune system

Abstract

Burkholderia pseudomallei is the causative agent of melioidosis. Currently no vaccines are available and not much is known about the mechanisms of adaptive immunity to the bacterium. In this project, in vitro systems were employed to study interactions of the bacteria with host T cells. B. pseudomallei is able to invade and replicate intracellularly in T cells and dendritic cells. We found that bacteria do not induce rapid cell death in infected T cells as in dendritic cells. In fact, bacterial infection modulates T cell function by enhancing IL-2 production upon the engagement of the T cell receptor. Further studies reveal bacterial flagellin as a potent costimulatory molecule of T cell activation. However, flagellin is not the major contributor to T cell costimulation during live bacterial infection as determined by flagellin null mutant bacteria. The direct coactivation of T cells by B. pseudomallei could contribute to severe inflammation seen in acutely-infected patients.