Emerging Insights into the Impact of Air Pollution on Immune-Mediated Asthma Pathogenesis

Abstract

Purpose of review: Increases in ambient levels of air pollutants have been linked to lung inflammation and remodeling, processes that lead to the development and exacerbation of allergic asthma. Conventional research has focused on the role of CD4⁺ T helper 2 (T_H2) cells in the pathogenesis of air pollution-induced asthma. However, much work in the past decade has uncovered an array of air pollution-induced non-T_H2 immune mechanisms that contribute to allergic airway inflammation and disease.

Recent findings: In this article, we review current research demonstrating the connection between common air pollutants and their downstream effects on non-T_H2 immune responses emerging as key players in asthma, including PRRs, ILCs, and non-T_H2 T cell subsets. We also discuss the proposed mechanisms by which air pollution increases immune-mediated asthma risk, including pre-existing genetic risk, epigenetic alterations in immune cells, and perturbation of the composition and function of the lung and gut microbiomes. Together, these studies reveal the multifaceted impacts of various air pollutants on innate and adaptive immune functions via genetic, epigenetic, and microbiome-based mechanisms that facilitate the induction and worsening of asthma.

Keywords: Air pollution; Asthma; Epigenetics; Innate lymphoid cells; Microbiome; T cells.

Fig. 1

Effects of air pollution on novel immune-mediated mechanisms of asthma pathogenesis. a Pollutants that induce or exacerbate asthma by altering immune-mediated responses. b Air pollution induced non-T_H2 immune responses, leading to increased susceptibility to or severity of asthma. c Mechanisms of pollutant-driven asthma pathogenesis, including genetic risk, epigenetic alterations, and changes in the lung/gut microbiome. Created with BioRender.com