Effects of Air Pollution on Lung Innate Lymphoid Cells: Review of In Vitro and In Vivo Experimental Studies.

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

doi:10.3390/ijerph16132347

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 (IFN-γ) 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.

Highlights

Air pollution exposure is associated with an array of respiratory problems, in children because their lungs and immune system are still maturing [1,2,3,4]
The search strategy was constructed in cooperation with a medical information specialist (Wichor M Bramer, Medical Library, Erasmus MC) and combined terms related to air pollution (e.g., “air pollution”, “carbon monoxide (CO)”, “diesel exhaust particles (DEP)”, “PM2.5”, or “O3”) with those related to ILCs (e.g., “innate lymphoid cells”, “ILC1”, “innate lymphoid cells type 2 (ILC2)”, “ILC3”, or “natural killer (NK)”), respiratory health (e.g., “asthma”, “respiratory infections”), or immunity (e.g., “innate immunity” or “cytokines”)
Out of the 12 remaining articles selected for the final evaluation, six studies investigated the effects of different pollutants on NK cells and six studies examined the effects on various other ILCs (Table 1)

Summary

Introduction

Air pollution exposure is associated with an array of respiratory problems, in children because their lungs and immune system are still maturing [1,2,3,4]. PM, DEP, O3 , and other chemicals and polluting compounds have been shown to have deleterious effects on the respiratory function of humans [3,5,6,7,8,10,11,12,13] Exposure to these outdoor environmental pollutants can result in acute airway inflammation [14,15], increased mucosal secretions [16], oxidative lung damage [17,18,19], and loss of antibacterial functions [20,21,22,23,24]. These conditions may be mediated by a harmful effect of the pollutants on lung immune cells

Methods

Results

Discussion

Conclusion