Air Pollution Particulate Matter Alters Antimycobacterial Respiratory Epithelium Innate Immunity

• DOI: 10.1128/iai.03018-14
• Publication Date: 2015-04-07T01:42:15Z
• Authors: César E. Rivas-Sa...; Srijata Sarkar; Pasquale Cantarella; Álvaro Osornio-Va...; Raúl Quintana-Bel...; Qingyu Meng; Thomas J. Kirn; Pamela Ohman Stri...; Judith C. Chow; John G. Watson; Martha Torres; Stephan Schwander
• Keywords: Air Pollutants; 0303 health sciences; DNA, Complementary; beta-Defensins; Mycobacterium tuberculosis; Respiratory Mucosa; Immunity, Innate; 3. Good health; 03 medical and health sciences; Gene Expression Regulation; 13. Climate action; Air Pollution; Cell Line, Tumor; 11. Sustainability; Humans; Particulate Matter; RNA, Messenger; Mexico

ABSTRACTInhalation 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 againstMycobacterium tuberculosishas 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 PM2.5or PM10deregulated the ability of the A549 cells to express the antimicrobial peptides human β-defensin 2 (HBD-2) and HBD-3 upon infection withM. tuberculosisand increased intracellularM. tuberculosisgrowth (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 enhancedM. tuberculosisgrowth represent mechanisms by which exposure to air pollution PM may increase the risk ofM. tuberculosisinfection and the development of TB.