Related Experiment Video
Updated: Apr 15, 2026

Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface
Published on: October 8, 2013
Air pollution particulate matter alters antimycobacterial respiratory epithelium innate immunity
César E Rivas-Santiago1, Srijata Sarkar1, Pasquale Cantarella1
1Rutgers School of Public Health, Department of Environmental and Occupational Health, Piscataway, New Jersey, USA.
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.
Insights
Air pollution particulate matter (PM) exposure impairs lung epithelial cells, reducing their ability to fight tuberculosis (TB). This increases Mycobacterium tuberculosis growth, potentially raising TB infection risk.
Area of Science:
- Environmental Health
- Immunology
- Microbiology
Background:
- Inhalation of indoor pollutants and cigarette smoke is linked to increased tuberculosis (TB) risk.
- The impact of ambient air pollution particulate matter (PM) on host immune responses against Mycobacterium tuberculosis is not well understood.
Purpose of the Study:
- To investigate how PM2.5 and PM10 affect innate immune responses in human alveolar epithelial cells against M. tuberculosis.
- To explore the mechanisms underlying PM-induced alterations in antimycobacterial defense.
Main Methods:
- Human alveolar type II epithelial cells (A549 cell line) were exposed to PM2.5 and PM10 from Mexico City.
- Antimicrobial peptide expression (HBD-2, HBD-3) and intracellular M. tuberculosis growth (CFU count) were measured.
- Cellular senescence and viability were assessed in PM-exposed cells.
Main Results:
- PM2.5 and PM10 exposure deregulated HBD-2 and HBD-3 expression in A549 cells upon M. tuberculosis infection.
- Exposure to PM2.5 and PM10 led to increased intracellular M. tuberculosis growth.
- PM exposure induced cellular senescence in A549 cells, independent of cell death.
Conclusions:
- PM exposure impairs epithelial cell defense against M. tuberculosis by downregulating antimicrobial peptides (HBD-2, HBD-3) and inducing senescence.
- These mechanisms may contribute to increased susceptibility to M. tuberculosis infection and TB development.
- Air pollution particulate matter poses a significant risk factor for TB pathogenesis.
More Related Videos
08:42Isolating Bronchial Epithelial Cells from Resected Lung Tissue for Biobanking and Establishing Well-Differentiated Air-Liquid Interface Cultures
Published on: May 26, 2023
10:26P. aeruginosa Infected 3D Co-Culture of Bronchial Epithelial Cells and Macrophages at Air-Liquid Interface for Preclinical Evaluation of Anti-Infectives
Published on: June 15, 2020
Related Concept Videos
Microbiota of the Respiratory Tract
Surface Membrane Barriers
The outer layer of the skin, the epidermis, is a robust barrier comprising layers of closely packed keratinized cells. This dense arrangement prevents microbes from penetrating the body. The periodic shedding of epidermal cells...
Transmission-based Precautions II: Airborne and Protective Environment
Airborne precautions:
Use airborne precautions when treating patients known or suspected to have diseases that spread through the air—for example, tuberculosis or measles. These organisms are present in smaller droplets expelled by an infected person and...
Atypical Pneumonia
Pulmonary Tuberculosis I
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
Defense Against Bacterial Pathogens
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...