Journal Article

Ozone-Induced Aryl Hydrocarbon Receptor Activation Controls Lung Inflammation via Interleukin-22 Modulation

Isabelle Maillet, Aurélie Couturier-Maillard, Louis Fauconnier, Florent Bataille, Dieudonnée Togbe, Harry Sokol, Marjolène Straube, Laure Dumoutier, Cyril Colas, Jacques van Snick, Valérie F. Quesniaux, Bernhard Ryffel, Chloé Michaudel

2020

Overview

Airborne ozone exposure causes severe lung injury and inflammation. The aryl hydrocarbon Receptor (AhR) (1), activated in pollutant-induced inflammation, is critical for cytokine production, especially IL-22 and IL-17A. The role of AhR in ozone-induced lung inflammation is unknown. We report here that chronic ozone exposure activates AhR with increased tryptophan and lipoxin A4 production in mice. AhR mice show increased lung inflammation, airway hyperresponsiveness, and tissue remodeling with an increased recruitment of IL-17A and IL-22-expressing cells in comparison to control mice. IL-17A- and IL-22-neutralizing antibodies attenuate lung inflammation in AhR and control mice. Enhanced lung inflammation and recruitment of ILC3, ILC2, and T cells were observed after T cell-specific AhR depletion using the AhR -deficient mice. Together, the data demonstrate that ozone exposure activates AhR, which controls lung inflammation, airway hyperresponsiveness, and tissue remodeling via the reduction of IL-22 expression.

• Publisher: Frontiers Media SA,Frontiers,Frontiers Media S.A
• Subject: [SDV]Life Sciences [q-bio] / AhR / Animals / Antibodies, Neutralizing / Antibodies, Neutralizing - immunology / Antibodies, Neutralizing - therapeutic use / Asthma / Basic Helix-Loop-Helix Transcription Factors / Basic Helix-Loop-Helix Transcription Factors - genetics / Basic Helix-Loop-Helix Transcription Factors - metabolism / Bataille F / CD4-Positive T-Lymphocytes / CD4-Positive T-Lymphocytes - immunology / Citation: Michaudel C / Colas C / Collagen / Couturier-Maillard A / Cytokines / Dumoutier L / Fauconnier L / Hydrocarbons / IL-17 / ILC3 / Immunologic diseases. Allergy / Immunology / Inflammation / Interleukin 22 / Interleukin-17 / Interleukin-17 - immunology / Interleukin-17 - metabolism / Interleukins / Interleukins - genetics / Interleukins - immunology / Interleukins - metabolism / Kinases / Life Sciences / Ligands / Lipoxin A4 / Lipoxins / Lipoxins - metabolism / Lung Injury / Lung Injury - chemically induced / Lung Injury - drug therapy / Lung Injury - metabolism / Lungs / Lymphocytes / Lymphocytes T / Maillet I / Metabolism / Metabolites / Mice / Mice, Inbred C57BL / Mice, Knockout / Neutrophils / Ozone / Ozone - adverse effects / Pneumonia / Pneumonia - chemically induced / Pneumonia - drug therapy / Pneumonia - metabolism / Pollutants / Proteins / Quesniaux VF / RC581-607 / Receptor mechanisms / Receptors, Aryl Hydrocarbon / Receptors, Aryl Hydrocarbon - genetics / Receptors, Aryl Hydrocarbon - metabolism / Receptors, Interleukin-17 / Receptors, Interleukin-17 - genetics / Respiratory Hypersensitivity / Respiratory Hypersensitivity - chemically induced / Respiratory Hypersensitivity - drug therapy / Respiratory Hypersensitivity - metabolism / Respiratory tract / Sokol H / Straube M / T cells / Togbe D and Ryffel B Ozone-Induced Aryl Hydrocarbon Receptor Activation Controls Lung Inflammation via Interleukin-22 Modulation / Tryptophan / Tryptophan - metabolism / van Snick J