Air Pollution Particulate Matter Alters Antimycobacterial Respiratory Epithelium Innate Immunity
Open accessAbstract
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 (PM 2.5 ) and 10 μm (PM 10 ) on innate antimycobacterial immune responses in human alveolar type II epithelial cells of the A549 cell line. Exposure to PM 2.5 or PM 10 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.
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Household air pollution, specifically particulate matter, can be involved in the reactivation of tuberculosis through impairing macrophage and respiratory epithelial cell function.
“From a biomedical perspective, HAP, specifically particulate matter, can be involved in the reactivation of TB through impairing macrophage and respiratory epithelial cell function, as shown in several studies,1316”
From Household air pollution exposure and risk of tuberculosis: a case–control study of women in Lilongwe, Malawi (2024) · cites this paper as [16]
It is not reasonable to conclude that there is no linkage between household air pollution from cooking with biomass and tuberculosis; rather, such a linkage is not detected in the study sample.
“Given the biomedical linkages between pollution, particularly PM and TB incidence1316 and the high levels of pollution emitted when combusting biomass cooking fuels, we do not think it is reasonable to conclude that there is no linkage between HAP from cooking with biomass and TB but rather that is not something we detect in our study sample.”
From Household air pollution exposure and risk of tuberculosis: a case–control study of women in Lilongwe, Malawi (2024) · cites this paper as [16]
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β-Defensins: Linking Innate and Adaptive Immunity Through Dendritic and T Cell CCR6
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Biomass fuel and risk of tuberculosis: a case–control study from Northern India
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PM2.5 Exposure and Asthma Development: The Key Role of Oxidative Stress
Liu, K., Hua, S., & Song, L. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/3618806 · Cited by 187 · see citing works
Pathak, A. K., Sharma, M., Katiyar, S. K., Katiyar, S., & Nagar, P. K. (2020) · Scientific Reports · doi:10.1038/s41598-020-79023-5 · Cited by 9 · see citing works
Jagger, P., McCord, R., Gallerani, A., Hoffman, I., Jumbe, C., Pedit, J., Phiri, S., Krysiak, R., & Maleta, K. (2024) · BMJ Public Health · doi:10.1136/bmjph-2023-000176 · Cited by 8 · see citing works
- Authors
- Rivas-Santiago, C. E., Sarkar, S., Cantarella, P., Osornio-Vargas, Á., Quintana-Belmares, R., Meng, Q., Kirn, T. J., Ohman Strickland, P., Chow, J. C., Watson, J. G., Torres, M., & Schwander, S.
- Affiliations
- Rutgers, The State University of New Jersey (US)
- University of Alberta (CA)
- Instituto Nacional de Cancerología (MX)
- Rutgers School of Public Health, Department of Biostatistics, Piscataway, New Jersey, USA
- Desert Research Institute (US)
- Instituto Nacional de Enfermedades Respiratorias (MX)
- ORCID
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 2015-06
- Volume
- 83
- Issue
- 6
- Pages
- 2507-2517
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC4432745
- OpenAlex
- W2154142324
- Cited by
- 150
- References
- 2
- Citations by year
- 2026: 9 · 2025: 16 · 2024: 14 · 2023: 21 · 2022: 19 · 2021: 18 · 2020: 22 · 2019: 13 · 2018: 9 · 2017: 5 · 2016: 2 · 2015: 2
- FWCI
- 4.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Infection and Immunity (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Environmental Health Sciences (R01ES020382, P30ES005022)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- PM2.5, PM10, tuberculosis, Mycobacterium tuberculosis, innate immunity, antimicrobial peptides, human beta-defensin 2, human beta-defensin 3, alveolar type II cells, A549 cells, cellular senescence, intracellular bacterial growth, indoor air pollution, cigarette smoke
- MeSH terms
- Air Pollutants, Air Pollution, Gene Expression Regulation, Humans, Immunity, Innate, Mexico, Mycobacterium tuberculosis, RNA, Messenger, DNA, Complementary, Respiratory Mucosa, beta-Defensins, Cell Line, Tumor, Particulate Matter
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