Consequences of acute ozone exposure imposed on the culminated allergic pulmonary inflammation in an established murine model of asthma

Bao, Ande; Li, Liang; Li, Feng; Zhang, Min; Zhou, Xin

doi:10.2741/4147

Cited by 17 publications

(13 citation statements)

References 59 publications

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“…Although there have been several similar mouse studies looking at the O 3 effects on the asthmatic inflammation [ 10 , 18 , 22 – 24 ], our work is unique in the animal protocol to mimic the real situation of O 3 -induced asthma exacerbation in human. It is worth to note that the concentration of O 3 used in this study (1.0 ppm) is relative higher than the atmosphere O 3 concentration (~0.01 ppm) for inducing a measurable biological response.…”

Section: Discussionmentioning

confidence: 99%

“…On day 28, all mice were placed in a whole-body plethysmography (Buxco™, NY) to measure enhanced pause (P enh ), as described previously [ 18 ]. The value was expressed as percentage change from baseline.…”

Section: Methodsmentioning

confidence: 99%

“…Lung sections (5 μm) were undergone hematoxylin and eosin (H&E) staining. The infiltration of inflammatory cells in peribronchial area and perivascular area were evaluated according to a 0~3 scoring system as previously described [ 18 , 21 ].…”

Section: Methodsmentioning

confidence: 99%

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Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model

Bao

Yang

et al. 2017

Respir Res

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BackgroundExposure to ambient ozone (O3) increases the susceptivity to allergens and triggers exacerbations in patients with asthma. However, the detailed mechanisms of action for O3 to trigger asthma exacerbations are still unclear.MethodsAn ovalbumin (OVA)-established asthmatic mouse model was selected to expose to filtered air (OVA-model) or 1.0 ppm O3 (OVA-O3 model) during the process of OVA challenge. Next, the possible involvements of p38 MAPK and oxidative stress in the ozone actions on the asthma exacerbations were investigated on the mice of OVA-O3 model by treating them with SB239063 (a p38 MAPK inhibitor), and/or the α-tocopherol (antioxidant). Biological measurements were conducted including airway hyperresponsiveness (AHR), airway resistance (Raw), lung compliance (CL), inflammation in the airway lumen and lung parenchyma, the phosphorylation of p38 MAPK and heat shock protein (HSP) 27 in the tracheal tissues, and the malondialdehyde (MDA) content and the glutathione peroxidase (GSH-Px) activity in lung tissues.ResultsIn OVA-allergic mice, O3 exposure deteriorated airway hyperresponsiveness (AHR), airway resistance (Raw), lung compliance (CL) and pulmonary inflammation, accompanied by the increased oxidative stress in lung tissues and promoted p38 MAPK and HSP27 phosphorylation in tracheal tissues. Administration of SB239063 (a p38 MAPK inhibitor) on OVA-O3 model exclusively mitigated the Raw, the CL, and the BAL IL-13 content, while α-tocopherol (antioxidant) differentially reduced the BAL number of eosinophils and macrophages, the content of BAL hyaluronan, the peribronchial inflammation, as well as the mRNA expression of TNF-α and IL-5 in the lung tissues of OVA-O3 model. Administration of these two chemical inhibitors similarly inhibited the AHR, the BAL IFN-γ and IL-6 production, the perivascular lung inflammation and the lung IL-17 mRNA expression of OVA-O3 model. Interestingly, the combined treatment of both compounds together synergistically inhibited neutrophil counts in the BALF and CXCL-1 gene expression in the lung.ConclusionsO3 exposure during the OVA challenge process promoted exacerbation in asthma. Both p38 MAPK and oxidative stress were found to play a critical role in this process and simultaneous inhibition of these two pathways significantly reduced the O3-elicited detrimental effects on the asthma exacerbation.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model

Bao

Yang

et al. 2017

Respir Res

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“…Real-time reverse transcription polymerase chain reaction (RT-PCR) was performed as previously described [ 18 ]. In brief, mRNA was prepared from homogenized tissues using a commercial Spin technology (RNeasy Mini ® , Qiagen ™ , MD) according to the manufacturer’s instructions and the purity verified using Nanodrop ® 2000 (Life Technology Inc ™ , CA).…”

Section: Methodsmentioning

confidence: 99%

Recombinant human IL-26 facilitates the innate immune response to endotoxin in the bronchoalveolar space of mice in vivo

et al. 2017

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Interleukin (IL)-26 is released in response to bacterial endotoxin (LPS) in the bronchoalveolar space of humans in vivo and it may potentiate neutrophil chemotaxis by enhanced IL-26 receptor stimulation. However, the effects of extracellular IL-26 protein on the innate immune response in the lungs in vivo remain unknown. Here, we characterized these effects of IL-26 on a wide range of aspects of the innate immune response to LPS in different compartments of the lungs in vivo over time. We administrated recombinant human (rh) IL-26 protein in the bronchoalveolar space using intranasal instillation in a mouse in vivo model, with and without prior instillation of LPS. We verified gene expression of the IL-26 receptor complex in mouse lungs and observed that, after instillation of LPS, rhIL-26 increases the phosphorylation of STAT3, a signaling molecule of the IL-26 receptor complex. We also observed that rhIL-26 exerted additional stimulatory and inhibitory actions that are compartment- and time-dependent, resulting in alterations of cytokines, proteinases, tissue inflammation and the accumulation of innate effector cells. Without the prior instillation of LPS, rhIL-26 exerted time-dependent effects on total gelatinase activity but few other effects. Most important, after instillation of LPS, rhIL-26 cleared inflammatory cells from local tissue and increased the accumulation of innate effector cells in the bronchoalveolar space. Tentatively, rhIL-26 may facilitate the innate immune response towards the bronchoalveolar space in vivo and represents a potential target for therapy in lung disorders involving the innate immune response.

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“…For example, a number of reports demonstrate that increased production hyaluronic acid is associated with various inflammatory conditions [9,10,11]. Under normal non-inflammatory conditions, hyaluronic acid exists primarily in its high molecular weight form (HMW-HA).…”

Section: Introductionmentioning

confidence: 99%

Treatment with the Hyaluronic Acid Synthesis Inhibitor 4-Methylumbelliferone Suppresses SEB-Induced Lung Inflammation

McKallip

Uchakina

2013

Toxins

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Exposure to bacterial superantigens, such as staphylococcal enterotoxin B (SEB), can lead to the induction of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). To date, there are no known effective treatments for SEB-induced inflammation. In the current study we investigated the potential use of the hyaluronic acid synthase inhibitor 4-methylumbelliferone (4-MU) on staphylococcal enterotoxin B (SEB) induced acute lung inflammation. Culturing SEB-activated immune cells with 4-MU led to reduced proliferation, reduced cytokine production as well as an increase in apoptosis when compared to untreated cells. Treatment of mice with 4-MU led to protection from SEB-induced lung injury. Specifically, 4-MU treatment led to a reduction in SEB-induced HA levels, reduction in lung permeability, and reduced pro-inflammatory cytokine production. Taken together, these results suggest that use of 4-MU to target hyaluronic acid production may be an effective treatment for the inflammatory response following exposure to SEB.

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Consequences of acute ozone exposure imposed on the culminated allergic pulmonary inflammation in an established murine model of asthma

Cited by 17 publications

References 59 publications

Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model

Involvements of p38 MAPK and oxidative stress in the ozone-induced enhancement of AHR and pulmonary inflammation in an allergic asthma model

Recombinant human IL-26 facilitates the innate immune response to endotoxin in the bronchoalveolar space of mice in vivo

Treatment with the Hyaluronic Acid Synthesis Inhibitor 4-Methylumbelliferone Suppresses SEB-Induced Lung Inflammation

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