Urban air pollution particulates suppress human t-cell responses to mycobacterium tuberculosis

Olufunmilola Ibironke, Claudia Carranza, Srijata Sarkar, Martha Torres, Hyejeong Theresa Choi, Joyce Nwoko, Kathleen Black, Raul Quintana-Belmares, Álvaro Osornio-Vargas, Pamela Ohman-Strickland, Stephan Schwander

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Tuberculosis (TB) and air pollution both contribute significantly to the global burden of disease. Epidemiological studies show that exposure to household and urban air pollution increase the risk of new infections with Mycobacterium tuberculosis (M.tb) and the development of TB in persons infected with M.tb and alter treatment outcomes. There is increasing evidence that particulate matter (PM) exposure weakens protective antimycobacterial host immunity. Mechanisms by which exposure to urban PM may adversely affect M.tb-specific human T cell functions have not been studied. We, therefore, explored the effects of urban air pollution PM2.5 (aerodynamic diameters ≤2.5µm) on M.tb-specific T cell functions in human peripheral blood mononuclear cells (PBMC). PM2.5 exposure decreased the capacity of PBMC to control the growth of M.tb and the M.tb-induced expression of CD69, an early surface activation marker expressed on CD3+ T cells. PM2.5 exposure also decreased the production of IFN-γ in CD3+, TNF-α in CD3+ and CD14+ M.tb-infected PBMC, and the M.tb-induced expression of T-box transcription factor TBX21 (T-bet). In contrast, PM2.5 exposure increased the expression of anti-inflammatory cytokine IL-10 in CD3+ and CD14+ PBMC. Taken together, PM2.5 exposure of PBMC prior to infection with M.tb impairs critical antimycobacterial T cell immune functions.

Original languageEnglish (US)
Article number4112
JournalInternational journal of environmental research and public health
Issue number21
StatePublished - Nov 2019

All Science Journal Classification (ASJC) codes

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis


  • Immunity
  • M.tb
  • PM
  • Proinflammatory cytokines
  • T-bet


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