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Infect Immun. 2015 Jun;83(6):2507-17. doi: 10.1128/IAI.03018-14. Epub 2015 Apr 6.

Air pollution particulate matter alters antimycobacterial respiratory epithelium innate immunity.

Author information

1
Rutgers School of Public Health, Department of Environmental and Occupational Health, Piscataway, New Jersey, USA.
2
Department of Pediatrics, University of Alberta, ECHA, Edmonton, AB, Canada.
3
Laboratory of Environmental Toxicology, Instituto Nacional de Cancerología, Mexico City, Mexico.
4
Rutgers School of Public Health, Department of Environmental and Occupational Health, Piscataway, New Jersey, USA Rutgers School of Public Health, Center for Global Public Health, Piscataway, New Jersey, USA.
5
Rutgers Robert Wood Johnson Medical School, Department of Pathology and Laboratory Medicine, New Brunswick, New Jersey, USA.
6
Rutgers School of Public Health, Department of Biostatistics, Piscataway, New Jersey, USA.
7
Desert Research Institute, Reno, Nevada, USA.
8
Department of Microbiology, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Tlalpan, Mexico City, Mexico.
9
Rutgers School of Public Health, Department of Environmental and Occupational Health, Piscataway, New Jersey, USA Rutgers School of Public Health, Center for Global Public Health, Piscataway, New Jersey, USA schwansk@sph.rutgers.edu.

Abstract

Inhalation exposure to indoor air pollutants and cigarette smoke increases the risk of developing tuberculosis (TB). Whether exposure to ambient air pollution particulate matter (PM) alters protective human host immune responses against Mycobacterium tuberculosis has been little studied. Here, we examined the effect of PM from Iztapalapa, a municipality of Mexico City, with aerodynamic diameters below 2.5 μm (PM2.5) and 10 μm (PM10) on innate antimycobacterial immune responses in human alveolar type II epithelial cells of the A549 cell line. Exposure to PM2.5 or PM10 deregulated the ability of the A549 cells to express the antimicrobial peptides human β-defensin 2 (HBD-2) and HBD-3 upon infection with M. tuberculosis and increased intracellular M. tuberculosis growth (as measured by CFU count). The observed modulation of antibacterial responsiveness by PM exposure was associated with the induction of senescence in PM-exposed A549 cells and was unrelated to PM-mediated loss of cell viability. Thus, the induction of senescence and downregulation of HBD-2 and HBD-3 expression in respiratory PM-exposed epithelial cells leading to enhanced M. tuberculosis growth represent mechanisms by which exposure to air pollution PM may increase the risk of M. tuberculosis infection and the development of TB.

PMID:
25847963
PMCID:
PMC4432745
DOI:
10.1128/IAI.03018-14
[Indexed for MEDLINE]
Free PMC Article

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