Ozone exposure induces respiratory barrier biphasic injury and inflammation controlled by IL-33

Michaudel, Chloé; Mackowiak, Claire; Maillet, Isabelle; Fauconnier, Louis; Akdiş, Cezmi A.; Sokołowska, Milena; Dreher, Anita; Tan, Hern‐Tze Tina; Quesniaux, Valérie; Ryffel, Bernhard; Togbé, Dieudonnée

doi:10.1016/j.jaci.2017.11.044

Cited by 97 publications

(105 citation statements)

References 71 publications

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“…Our previous studies showed that ozone could induce airway obstruction in a concentration-dependent manner, 17,18 and alveolar epithelial proliferation and nitric oxide synthase be involved in airway bstruction in mice exposed to ozone. [17][18][19][20][21] The long-term ozone exposure cause to the ratio of IL-4 to INF-gamma and increase in numbers of goblet FIG URE 6 Ozone increased antioxidant response and cytokine levels. A, IL-1b, IL-18, TNF-a, and IL-4 concentrations were increased after ozone exposure.…”

Section: Discussionmentioning

confidence: 96%

“…Our previous studies showed that ozone could induce airway obstruction in a concentration‐dependent manner, and alveolar epithelial proliferation and nitric oxide synthase be involved in airway bstruction in mice exposed to ozone . The long‐term ozone exposure cause to the ratio of IL‐4 to INF‐gamma and increase in numbers of goblet cells, myofibroblasts, and smooth muscle cells, indicating that prolonged ozone exposure lead to airway remodeling . However, the relationship between ozone exposure and epithelial tight junctions remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…IL‐4 increased in bronchoalveolar lavage fluid in ozone exposure model. More studies will be needed to clarify the biological mechanisms of the interaction between ozone exposure and TH1 and TH2 cytokines for tight junction proteins …”

Section: Discussionmentioning

confidence: 99%

“…*P < .05 ozone versus air controls cells, myofibroblasts, and smooth muscle cells, indicating that prolonged ozone exposure lead to airway remodeling. [17][18][19][20][21][22][23][24] However, the relationship between ozone exposure and epithelial tight junctions remains unclear. In this study, we examined the role of CLDNs in ozone exposure mouse model and primary human lung epithelial cells, which provided persuasive evidence for the mechanism for asthma exacerbation due to ozone.…”

Section: Discussionmentioning

confidence: 99%

“…1,25 Epidemiological data indicate that individuals with chronic inflammatory diseases, such as asthma or chronic obstructive pulmonary disease, are hypersensitive to ozone, exhibiting increased morbidity and mortality. 17,26,27 Acute inhalation of ozone causes structural alterations in the lung, including disruption of the alveolar epithelial barrier that leads to alveolar epithelial type II cell hypertrophy and hyperplasia. 16,28 Recruitment of inflammatory cells into the lung following ozone exposure presents another risk for tissue damage through the release of toxic mediators from activated macrophages and neutrophils, including cytokines, 23,24 reactive oxygen and nitrogen species, 21 and proteolytic enzymes.…”

Section: Discussionmentioning

confidence: 99%

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Impact of ozone on claudins and tight junctions in the lungs

Kim

Lee

et al. 2018

Environmental Toxicology

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Claudins (CLDNs) are a major transmembrane protein component of tight junctions (TJs) in endothelia and epithelia. CLDNs are not only essential for sustaining the role of TJs in cell permeability but are also vital for cell signaling through protein-protein interactions. Ozone induces oxidative stress and lung inflammation in humans and experimental models, but the impact of ozone on claudins remains poorly understood. This study was to determine the expression of TJ proteins, such as claudin 3, 4, 5, and 14 following ozone exposure. Mice were exposed to 0.1, 1, or 2 ppm of ozone or ambient air for 6 h for 3 days. The impact of ozone on CLDNs, Nrf2, Keap1, and reactive oxygen species (ROS) were estimated using immunoblotting, immunohistochemical staining, confocal imaging, and ELISA analysis in mice and bronchial epithelial cells. Mice exposed to ozone experienced increased airway inflammatory cell infiltration and bronchial hyper-responsiveness compared to control mice. Additionally, CLDN3, CLDN4, ROS, Nrf2, and Keap1 protein expression increased, and lung CLDN14 protein expression decreased, in mice exposed to ozone compared with control mice. These results indicate that CLDNs are involved in airway inflammation following ozone exposure, suggesting that ozone affects TJ proteins through oxidative mechanisms.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Impact of ozone on claudins and tight junctions in the lungs

Kim

Lee

et al. 2018

Environmental Toxicology

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The contribution of animal models to understanding the role of the immune system in human idiopathic pulmonary fibrosis

et al. 2020

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Pulmonary fibrosis occurs in a heterogeneous group of lung disorders and is characterised by an excessive deposition of extracellular matrix proteins within the pulmonary interstitium, leading to impaired gas transfer and a loss of lung function. In the past 10 years, there has been a dramatic increase in our understanding of the immune system and how it contributes to fibrogenic processes within the lung. This review will compare some of the models used to investigate the pathogenesis and treatment of pulmonary fibrosis, in particular those used to study immune cell pathogenicity in idiopathic pulmonary fibrosis, highlighting their advantages and disadvantages in dissecting human disease.

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IL‐33/ST2 axis deficiency exacerbates neutrophil‐dominant allergic airway inflammation

Qian

Jiang

et al. 2021

Clin & Trans Imm

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Objective The IL‐33/ST2 axis has been extensively investigated in type 2 eosinophilic inflammation. Here, we aimed to investigate the role of the IL‐33/ST2 axis in neutrophil‐dominant allergic airway inflammation. Methods House‐dust mite (HDM) extract and lipopolysaccharide (LPS) were administered to establish a murine model of neutrophil‐dominant allergic airway inflammation. The formation of neutrophilic extracellular traps (NETs) in the lung tissues was demonstrated by immunofluorescence imaging. Mature IL‐33 in bronchoalveolar lavage fluid (BALF) was detected by Western blotting. The neutrophilic chemokine KC produced by bone marrow‐derived macrophages (BMDMs) or primary alveolar epithelial cells was measured with a commercial ELISA kit. Results In the present study, we observed neutrophilic inflammation and tight junction damage in the lungs of mice sensitised with HDM and LPS. Furthermore, sensitisation with HDM and LPS resulted in the formation of NETs, accompanied by increased levels of mature IL‐33 in the BALF. Moreover, LPS damaged the epithelial tight junction protein occludin directly or indirectly by inducing NET formation. Surprisingly, IL‐33 deficiency augmented neutrophilia and epithelial barrier injury in the lungs of mice after sensitisation with HDM and LPS. Similarly, the absence of ST2 exacerbated the neutrophilic inflammatory response, decreased the expression of occludin and exacerbated the severity of neutrophil‐dominant allergic airway inflammation in an HDM/LPS‐induced mouse model. Mechanistically, BMDMs and alveolar epithelial cells from IL‐33‐ or ST2‐deficient mice tended to produce higher levels of the neutrophilic chemokine KC. Conclusions These results demonstrated that the IL‐33/ST2 axis may play a protective role in neutrophil‐dominant allergic airway inflammation.

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Ozone exposure induces respiratory barrier biphasic injury and inflammation controlled by IL-33

Abstract: Data demonstrate that ozone causes an immediate barrier injury that precedes myeloid cell-mediated inflammatory injury under the control of the IL-33/ST2 axis. Thus IL-33/ST2 signaling is critical for maintenance of intact epithelial barrier and inflammation.

Cited by 97 publications

References 71 publications

Impact of ozone on claudins and tight junctions in the lungs

Impact of ozone on claudins and tight junctions in the lungs

The contribution of animal models to understanding the role of the immune system in human idiopathic pulmonary fibrosis

IL‐33/ST2 axis deficiency exacerbates neutrophil‐dominant allergic airway inflammation

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