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.

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.

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