Open AccessExperimental exposure of Burkholderia pseudomallei crude culture filtrate upregulates PD-1 on T lymphocytes
Author(s) -
Nivedita Me,
Vanitha Mariappan,
Kumutha Malar Vellasamy,
Chandramathi Samudi,
Jia-Xiang See,
P. Sankar Ganesh,
Alireza Saeidi,
Jamuna Vadivelu,
Esaki M. Shankar
Publication year - 2020
Publication title -
access microbiology
Language(s) - English
Resource type - Journals
ISSN - 2516-8290
DOI - 10.1099/acmi.0.000110
Subject(s) - burkholderia pseudomallei , melioidosis , microbiology and biotechnology , biology , pathogenesis , downregulation and upregulation , immune system , bacteria , flow cytometry , multiplicity of infection , incubation , intracellular , in vitro , immunology , gene , biochemistry , genetics
Burkholderia pseudomalleiis the causative agent for melioidosis. Because of its intracellular nature, the bacterium is capable of replicating within a plethora of eukaryotic cell lines.B. pseudomalleican remain dormant within host cells without symptoms for years, causing recrudescent infections. Here, we investigated the pathogenesis mechanism behind the suppression of T cell responses byB. pseudomallei . Peripheral blood mononuclear cells (1×10 6 cells/well) isolated by Ficoll Paque (Sigma-Aldrich) density gradient centrifugation were incubated with optimized concentrations of bacterial crude culture filtrate antigens (CFAs) (10 ug ml −1 ) and heat-killed bacteria [1 : 10 multiplicity of infection (m.o.i.)]. Following incubation, cells were investigated for surface expression of coinhibitory molecules by flow cytometry. We found thatB. pseudomalleiinduced the upregulation of programmed death 1 (PD-1), a molecule responsible for T cell exhaustion, on T cells in vitro following exposure to crude CFAs ofB. pseudomallei . This upregulation of PD-1 probably contributes to poor immune surveillance and disease pathogenesis.