Urban Air Pollution Particulates Suppress Human T-Cell Responses to Mycobacterium Tuberculosis.
Olufunmilola IbironkeClaudia CarranzaSrijata SarkarMartha TorresHyejeong Theresa ChoiJoyce NwokoKathleen BlackRaul Quintana-BelmaresAlvaro R Osornio-VargasPamela Ohman-StricklandStephan SchwanderPublished in: International journal of environmental research and public health (2019)
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.
Keyphrases
- air pollution
- mycobacterium tuberculosis
- particulate matter
- lung function
- pulmonary tuberculosis
- endothelial cells
- transcription factor
- poor prognosis
- magnetic resonance
- rheumatoid arthritis
- heavy metals
- immune response
- long non coding rna
- polycyclic aromatic hydrocarbons
- chronic obstructive pulmonary disease
- oxidative stress
- diabetic rats
- dendritic cells
- risk assessment
- cystic fibrosis
- human immunodeficiency virus
- hiv infected
- hiv aids