Urban Air Pollution Particulates Suppress Human T-Cell Responses to Mycobacterium Tuberculosis

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 (M.tb) and the development of TB in persons infected with and alter treatment ou...

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Veröffentlicht in:International journal of environmental research and public health 2019-10, Vol.16 (21), p.4112
Hauptverfasser: Ibironke, Olufunmilola, Carranza, Claudia, Sarkar, Srijata, Torres, Martha, Choi, Hyejeong Theresa, Nwoko, Joyce, Black, Kathleen, Quintana-Belmares, Raul, Osornio-Vargas, Álvaro, Ohman-Strickland, Pamela, Schwander, Stephan
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Sprache:eng
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Zusammenfassung: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 (M.tb) and the development of TB in persons infected with 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 -specific human T cell functions have not been studied. We, therefore, explored the effects of urban air pollution (aerodynamic diameters ≤2.5µm) on M.tb-specific T cell functions in human peripheral blood mononuclear cells (PBMC). 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. 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, exposure increased the expression of anti-inflammatory cytokine IL-10 in CD3 and CD14 PBMC. Taken together, exposure of PBMC prior to infection with M.tb impairs critical antimycobacterial T cell immune functions.
ISSN:1660-4601
1661-7827
1660-4601
DOI:10.3390/ijerph16214112