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

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

doi:10.3389/fimmu.2020.00144

Cited by 38 publications

(41 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chronic O 3 exposure has been suggested to activate AhR via production of lipoxin A4, which regulates lung inflammation and epithelial damage after exposure and promotes T H 2 and T H 17 responses. 238 In human subjects, O 3 exposure is believed to enhance pulmonary immunity and promote allergic responses. 48 Since O 3 is instantaneously consumed, unlike PM, allergic responses are believed to be triggered by secondary messengers, such as IL-33.…”

Section: Effects Of Pollutant Exposure On Adaptive Immune Responsesmentioning

confidence: 99%

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

Woodby

Arnold

Valacchi

2020

Annals of the New York Academy of Sciences

126

113

View full text Add to dashboard Cite

Exposure to air pollutants has been previously associated with respiratory viral infections, including influenza, measles, mumps, rhinovirus, and respiratory syncytial virus. Epidemiological studies have also suggested that air pollution exposure is associated with increased cases of SARS-CoV-2 infection and COVID-19-associated mortality, although the molecular mechanisms by which pollutant exposure affects viral infection and pathogenesis of COVID-19 remain unknown. In this review, we suggest potential molecular mechanisms that could account for this association. We have focused on the potential effect of exposure to nitrogen dioxide (NO 2), ozone (O 3), and particulate matter (PM) since there are studies investigating how exposure to these pollutants affects the life cycle of other viruses. We have concluded that pollutant exposure may affect different stages of the viral life cycle, including inhibition of mucociliary clearance, alteration of viral receptors and proteases required for entry, changes to antiviral interferon production and viral replication, changes in viral assembly mediated by autophagy, prevention of uptake by macrophages, and promotion of viral spread by increasing epithelial permeability. We believe that exposure to pollutants skews adaptive immune responses toward bacterial/allergic immune responses, as opposed to antiviral responses. Exposure to air pollutants could also predispose exposed populations toward developing COIVD-19associated immunopathology, enhancing virus-induced tissue inflammation and damage.

show abstract

Section: Effects Of Pollutant Exposure On Adaptive Immune Responsesmentioning

confidence: 99%

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

Woodby

Arnold

Valacchi

2020

Annals of the New York Academy of Sciences

126

113

View full text Add to dashboard Cite

show abstract

“…[ 24 ] Especially, depletion in T cell‐specific AhR is accompanied by the enhanced recruitment of innate lymphoid cells and T cells. [ 30 ] Besides, 5‐HT pathway also influenced the maturation and proliferation of immune cells through various 5‐HT receptors (5‐HTRs) and thus promoted the formation of inflammatory cytokines. [ 31 ] Therefore, the objectives of this review are to explore the complex mechanisms and interrelationships of the three major Trp catabolism pathways in controlling inflammation and the potential function of dietary Trp in ameliorating IBD.…”

Section: Introductionmentioning

confidence: 99%

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

Zhang

Zabed

et al. 2021

Molecular Nutrition Food Res

View full text Add to dashboard Cite

Inflammatory bowel disease (IBD) is complex, chronic, and relapsing gastrointestinal inflammatory disorders, which includes mainly two conditions, namely ulcerative colitis (UC) and Crohn's disease (CD). Development of IBD in any individual is closely related to his/her autoimmune regulation, gene‐microbiota interactions, and dietary factors. Dietary tryptophan (Trp) is an essential amino acid for intestinal mucosal cells, and it is associated with the intestinal inflammation, epithelial barrier, and energy homeostasis of the host. According to recent studies, Trp and its three major metabolic pathways, namely kynurenine (KYN) pathway, indole pathway, and 5‐hydroxytryptamine (5‐HT) pathway, have vital roles in the regulation of intestinal inflammation by acting directly or indirectly on the pro/anti‐inflammatory cytokines, functions of various immune cells, as well as the intestinal microbial composition and homeostasis. In this review, recent advances in Trp‐ and its metabolites‐associated intestinal inflammation are summarized. It further discusses the complex mechanisms and interrelationships of the three major metabolic pathways of Trp in regulating inflammation, which could elucidate the value of dietary Trp to be used as a nutrient for IBD patients.

show abstract

“…The beneficial role of AhR on T cell activity modulation was also demonstrated in another study evaluating ozone, an air pollutant that causes respiratory inflammation and exacerbates asthma. Upon chronic ozone exposure in mice, Ahr is activated in the lung, and lipoxin A4, an anti-inflammatory molecule and AhR ligand [ 19 ] is released in broncho-alveolar lavage fluids [ 20 ]. In this model, Ahr -deficient mice exhibited an increase in cell recruitment, airway hyperreactivity, epithelial cell injury, inflammation, and fibrosis suggesting that Ahr regulates lung inflammation and epithelial damage after ozone exposure [ 20 ].…”

Section: Ahr and Its Beneficial Effects In Experimental Asthmamentioning

confidence: 99%

“…Upon chronic ozone exposure in mice, Ahr is activated in the lung, and lipoxin A4, an anti-inflammatory molecule and AhR ligand [ 19 ] is released in broncho-alveolar lavage fluids [ 20 ]. In this model, Ahr -deficient mice exhibited an increase in cell recruitment, airway hyperreactivity, epithelial cell injury, inflammation, and fibrosis suggesting that Ahr regulates lung inflammation and epithelial damage after ozone exposure [ 20 ]. The expression of Ahr in T cells was necessary to control ozone-induced lung inflammatory cell infiltration, as shown in mice with a T cell-specific Ahr deletion.…”

Section: Ahr and Its Beneficial Effects In Experimental Asthmamentioning

confidence: 99%

“…For Il-17, Ahr acted directly on cell production and indirectly on cell recruitment. Lastly, Il-17- and Il-22- neutralizing antibodies attenuated lung inflammation in Ahr −/− and control mice [ 20 ]. Therefore, ozone exposure activates Ahr, which plays a beneficial role in controlling ozone-induced lung inflammation and airway hyperresponsiveness via the reduction of Th17 cytokine expression.…”

Section: Ahr and Its Beneficial Effects In Experimental Asthmamentioning

confidence: 99%

See 1 more Smart Citation

The Aryl Hydrocarbon Receptor in Asthma: Friend or Foe?

Poulain‐Godefroy

Bouté

Carrard

et al. 2020

IJMS

View full text Add to dashboard Cite

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that has emerged as an important player in asthma control. AhR is responsive to environmental molecules and endogenous or dietary metabolites and regulates innate and adaptive immune responses. Binding of this receptor by different ligands has led to seemingly opposite responses in different asthma models. In this review, we present two sides of the same coin, with the beneficial and deleterious roles of AhR evaluated using known endogenous or exogenous ligands, deficient mice or antagonists. On one hand, AhR has an anti-inflammatory role since its activation in dendritic cells blocks the generation of pro-inflammatory T cells or shifts macrophages toward an anti-inflammatory M2 phenotype. On the other hand, AhR activation by particle-associated polycyclic aromatic hydrocarbons from the environment is pro-inflammatory, inducing mucus hypersecretion, airway remodelling, dysregulation of antigen presenting cells and exacerbates asthma features. Data concerning the role of AhR in cells from asthmatic patients are also reviewed, since AhR could represent a potential target for therapeutic immunomodulation.

show abstract

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

Cited by 38 publications

References 68 publications

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

The Aryl Hydrocarbon Receptor in Asthma: Friend or Foe?

Contact Info

Product

Resources

About