Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation

Michaudel, Chloé; Maillet, Isabelle; Fauconnier, Louis; Quesniaux, Valérie; Chung, Kian Fan; Wiegman, Coen; Peter, Daniel; Ryffel, Bernhard

doi:10.3389/fimmu.2018.00916

Cited by 25 publications

(21 citation statements)

References 40 publications

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“…The severity of lung inflammation in peribronchial and perivascular in H&E sections was scored on a scale ranging from 0 to 3 where 0 means no inflammation; 1 means mild inflammation with only a few inflammatory cells around bronchial or vascular wall and in alveolar space; 2 means moderate inflammation with patchy inflammatory cells infiltration or localized inflammation around bronchial or vascular wall and in alveolar space and less than one-third of lung cross-sectional area involved; 3 means severe inflammation with diffuse inflammatory cells infiltration and more than one-third of the lung area involved. The scale was made referred to similar study 53 .…”

Section: Histological Analysismentioning

confidence: 99%

TRPC6-dependent Ca2+ signaling mediates airway inflammation in response to oxidative stress via ERK pathway

Chen

Zhou

et al. 2020

Cell Death Dis

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Ozone (O 3) plays an extremely important role in airway inflammation by generating reactive oxygen species (ROS) including hydrogen peroxide, then promoting redox actions and causing oxidative stress. Evidences indicate that TRPC6 (canonical transient receptor potential channel 6) is a redox-regulated Ca 2+ permeable nonselective cation channel, but its role in the setting of oxidative stress-related airway inflammation remains unknown. Here, we found that both TRPC6 −/− mice and mice pretreated with SAR7334, a potent TRPC6 inhibitor, were protected from O 3-induced airway inflammatory responses. In vitro, both knockdown of TRPC6 expression with shRNA and TRPC6 blockage markedly attenuated the release of cytokines IL-6 and IL-8 induced by O 3 or H 2 O 2 in 16HBE cells (human bronchial epithelial cell line). Treatment with O 3 or H 2 O 2 enhanced TRPC6 protein expression in vivo and vitro. We also observed that TRPC6-dependent increase of intracellular Ca 2+ concentration ([Ca 2+ ] i) was triggered by H 2 O 2 , which consisted of the release from intracellular calcium store and the influx of extracellular Ca 2+ and could be further strengthened by 6-h O 3 exposure in both 16HBE cells and HBEpiCs (primary human bronchial epithelial cells). Moreover, we confirmed that the activation of MAPK signals (ERK1/2, p38, JNK) was required for the inflammatory response induced by O 3 or H 2 O 2 while only the phosphorylation of ERK pathway was diminished in the TRPC6knockdown situation. These results demonstrate that oxidative stress regulates TRPC6-mediated Ca 2+ cascade, which leads to the activation of ERK pathway and inflammation and could become a potential target to treat oxidative stressassociated airway inflammatory diseases.

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Section: Histological Analysismentioning

confidence: 99%

TRPC6-dependent Ca2+ signaling mediates airway inflammation in response to oxidative stress via ERK pathway

Chen

Zhou

et al. 2020

Cell Death Dis

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“…The ozone-induced oxidative stress response might be involved in the activation of the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome complex ( 51 ). Both the acute and chronic exposure of mice to ozone induces lung inflammation through activation of ROS and of the NLRP3 inflammasome with caspase activation ( 52 , 53 ) and release of the highly inflammatory mediator IL-1β, but also IL-1α ( 54 ), which are involved in the ozone injury response ( 55 ). Uric acid crystals cause NLRP3-dependent lung inflammation upon injury ( 56 ) and therefore it is not excluded that crystals formed during injury may contribute to ozone induced inflammation ( 57 ).…”

Section: Mechanisms Of Ozone-induced Oxidative Stress On Inflammationmentioning

confidence: 99%

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

et al. 2020

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Oxidative stress plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD) caused by cigarette smoke and characterized by chronic inflammation, alveolar destruction (emphysema) and bronchiolar obstruction. Ozone is a gaseous constituent of urban air pollution resulting from photochemical interaction of air pollutants such as nitrogen oxide and organic compounds. While acute exposure to ozone induces airway hyperreactivity and neutrophilic inflammation, chronic ozone exposure in mice causes activation of oxidative pathways resulting in cell death and a chronic bronchial inflammation with emphysema, mimicking cigarette smoke-induced COPD. Therefore, the chronic exposure to ozone has become a model for studying COPD. We review recent data on mechanisms of ozone induced lung disease focusing on pathways causing chronic respiratory epithelial cell injury, cell death, alveolar destruction, and tissue remodeling associated with the development of chronic inflammation and AHR. The initial oxidant insult may result from direct effects on the integrity of membranes and organelles of exposed epithelial cells in the airways causing a stress response with the release of mitochondrial reactive oxygen species (ROS), DNA, and proteases. Mitochondrial ROS and mitochondrial DNA activate NLRP3 inflammasome and the DNA sensors cGAS and STING accelerating cell death pathways including caspases with inflammation enhancing alveolar septa destruction, remodeling, and fibrosis. Inhibitors of mitochondrial ROS, NLRP3 inflammasome, DNA sensor, cell death pathways, and IL-1 represent novel therapeutic targets for chronic airways diseases underlined by oxidative stress.

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“…The final antimicrobial effect of the ozone therapy lies in activation of specific antibodies. 39 The theoretically predicted major analgesic e��ect o� ozone was confirmed on biological models. Subcutane� ous administration o� o�ygen�ozone mi�ture to mice (a neuropathic pain model) prevented the emergence o� allo� dynia and reduced the concentration of pro-inflammatory enzymes in the orbito�rontal corte�.…”

Section: Ozone Therapy Mechanismmentioning

confidence: 76%

Analgetic effect of ozone therapy: myths of reality?

et al. 2020

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Introduction: Administration of an oxygen-ozone mixture is one of the innovative techniques used in single-drug or complex therapeutic schemes for treatment of many degenerative-dystrophic pathologies of the musculoskeletal system and related neurological complications. Aim: The aim was to determine the mechanisms of physiological action of the oxygen-ozone mixture in order to substantiate its efficacy for treatment of chronic pain syndrome with underlying degenerative-dystrophic pathologies of the musculoskeletal system. Material and methods: The article covers biochemical and pathomorphological studies that explain the mechanism of the pain syndrome and the potential effect of the ozone therapy. Results and discussion: The treatment schemes and benefits of different routes of ozone administration (intramuscularly, intravenously, intradiscally and intraarticularly) were analyzed. Diverse research data demonstrated influence on the causes of chronic pain, pathophysiological phases, and possible complications. The prospects of further studies for development of the most effective techniques for treatment of various pain syndromes were assessed. Conclusions: Ozone therapy is one of the alternative rehabilitation methods with a substantial pain relieving effect. As of today, the possibility of using the oxygen-ozone mixture for treatment of chronic back pain related to intervertebral disk hernia and fibromyalgia has been substantially confirmed.

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Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation

Cited by 25 publications

References 40 publications

TRPC6-dependent Ca2+ signaling mediates airway inflammation in response to oxidative stress via ERK pathway

TRPC6-dependent Ca2+ signaling mediates airway inflammation in response to oxidative stress via ERK pathway

Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease

Analgetic effect of ozone therapy: myths of reality?

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