Effects of air pollution on lung innate lymphoid cells: Review of in vitro and in vivo experimental studies

  • Bertha Estrella
  • , Elena N. Naumova
  • , Magda Cepeda
  • , Trudy Voortman
  • , Peter D. Katsikis
  • , Hemmo A. Drexhage

Research output: Contribution to journalReview articlepeer-review

35 Scopus citations

Abstract

Outdoor air pollution is associated with respiratory infections and allergies, yet the role of innate lymphoid cells (ILCs) in pathogen containment and airway hyperresponsiveness relevant to effects of air pollutants on ILCs is poorly understood. We conducted a systematic review to evaluate the available evidence on the effect of outdoor air pollutants on the lung type 1 (ILC1) and type 2 ILCs (ILC2) subsets. We searched five electronic databases (up to Dec 2018) for studies on the effect of carbon monoxide (CO), sulfur dioxide (SO2), nitrogen dioxide (NO2), diesel exhaust particles (DEP), ozone (O3), and particulate matter (PM) on respiratory ILCs. Of 2209 identified citations, 22 full-text papers were assessed for eligibility, and 12 articles describing experimental studies performed in murine strains (9) and on human blood cells (3) were finally selected. Overall, these studies showed that exposure to PM, DEP, and high doses of O3 resulted in a reduction of interferon gamma (IFNγ) production and cytotoxicity of ILC1. These pollutants and carbon nanotubes stimulate lung ILC2s, produce high levels of interleukin (IL)-5 and IL-13, and induce airway hyperresponsiveness. These findings highlight potential mechanisms by which human ILCs react to air pollution that increase the susceptibility to infections and allergies.

Original languageEnglish
Article number2347
JournalInternational Journal of Environmental Research and Public Health
Volume16
Issue number13
DOIs
StatePublished - 01 Jul 2019
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Air pollutants
  • Airway hyperresponsiveness
  • ILC
  • Lung innate lymphoid cells

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