Year in review 2017: Chronic obstructive pulmonary disease and asthma

Benton, Melissa J.; Lim, Tow Keang; Ko, Fanny Wai San; Kan-o, Keiko; Mak, Judith C.W.

doi:10.1111/resp.13285

Cited by 7 publications

(10 citation statements)

References 81 publications

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“…Currently affecting more than 200 million individuals worldwide, COPD manifests as a progressive damage to the pulmonary integrity with various clinical symptoms and complicated pathophysiological mechanisms (Caramori et al, 2017 ; Benton et al, 2018 ). Abnormal immune responses and severe inflammation in the lung airways are closely related to the initiation and progression of COPD.…”

Section: Approved Pde4 Inhibitors For the Treatment Of Inflammatory Dmentioning

confidence: 99%

“…Furthermore, available evidence indicated that the neutrophil-to-lymphocyte ratio (NLR) might predict the progression and outcomes of COPD (Paliogiannis et al, 2018 ). Asthma is another refractory inflammatory airway disease, which is characterized by bronchial hyperreactivity, mucus production, airway narrowing, and remodeling, along with explosion of inflammatory cells, especially neutrophils (Gao et al, 2017 ; Benton et al, 2018 ; Castro-Rodriguez et al, 2018 ). Undoubtedly, COPD and asthma patients share similar clinical phenotypes, and it is difficult to distinguish asthma from COPD, particularly when they coexist in elderly patients (Tochino et al, 2017 ).…”

Section: Approved Pde4 Inhibitors For the Treatment Of Inflammatory Dmentioning

confidence: 99%

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Phosphodiesterase-4 Inhibitors for the Treatment of Inflammatory Diseases

2018

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Phosphodiesterase-4 (PDE4), mainly present in immune cells, epithelial cells, and brain cells, manifests as an intracellular non-receptor enzyme that modulates inflammation and epithelial integrity. Inhibition of PDE4 is predicted to have diverse effects via the elevation of the level of cyclic adenosine monophosphate (cAMP) and the subsequent regulation of a wide array of genes and proteins. It has been identified that PDE4 is a promising therapeutic target for the treatment of diverse pulmonary, dermatological, and severe neurological diseases. Over the past decades, numerous PDE4 inhibitors have been designed and synthesized, among which roflumilast, apremilast, and crisaborole were approved for the treatment of inflammatory airway diseases, psoriatic arthritis, and atopic dermatitis, respectively. It is regrettable that the dramatic efficacies of a drug are often accompanied by adverse effects, such as nausea, emesis, and gastrointestinal reactions. However, substantial advances have been made to mitigate the adverse effects and obtain better benefit-to-risk ratio. This review highlights the dialectical role of PDE4 in drug discovery and the disquisitive details of certain PDE4 inhibitors to provide an overview of the topics that still need to be addressed in the future.

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Section: Approved Pde4 Inhibitors For the Treatment Of Inflammatory Dmentioning

confidence: 99%

Section: Approved Pde4 Inhibitors For the Treatment Of Inflammatory Dmentioning

confidence: 99%

Phosphodiesterase-4 Inhibitors for the Treatment of Inflammatory Diseases

2018

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“…Asthma is a chronic disease affecting 235 million people worldwide. The disease is characterized by airway hyperresponsiveness, airway narrowing and airway inflammation containing high numbers of eosinophils ( 1 , 2 ). House dust mite (HDM) is a common allergen that can induce allergic diseases like asthma and allergic rhinitis ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

The Combination Therapy of Dietary Galacto-Oligosaccharides With Budesonide Reduces Pulmonary Th2 Driving Mediators and Mast Cell Degranulation in a Murine Model of House Dust Mite Induced Asthma

et al. 2018

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Background: Dietary non-digestible galacto-oligosaccharides (GOS) suppress allergic responses in mice sensitized and challenged with house dust mite (HDM). Budesonide is the standard therapy for allergic asthma in humans but is not always completely effective.Aim: To compare the efficacy of budesonide or different doses of GOS alone or with a combination therapy of budesonide and GOS on HDM-allergic responses in mice.Methods:BALB/c mice were sensitized and challenged with HDM, while fed a control diet or a diet supplemented with 1 or 2.5 w/w% GOS, and either or not oropharyngeally instilled with budesonide. Systemic and local inflammatory markers, such as mucosal mast cell protease-1 (mMCP-1) in serum, pulmonary CCL17, CCL22, and IL-33 concentrations and inflammatory cell influx in the bronchoalveolar lavage fluid (BALF) were determined.Results: Budesonide or GOS alone suppressed the number of eosinophils in the BALF of HDM allergic mice whereas budesonide either or not combined with GOS lowered both eosinophil and lymphocyte numbers in the BALF of HDM-allergic mice. Both 1 w/w% and 2.5 w/w% GOS and/or budesonide suppressed serum mMCP-1 concentrations. However, budesonide nor GOS alone was capable of reducing Th2 driving chemokines CCL17, CCL22 and IL-33 protein levels in supernatants of lung homogenates of HDM allergic mice, whereas the combination therapy did. Moreover, IL-13 concentrations were only significantly suppressed in mice treated with budesonide while fed GOS. A similar tendency was observed for the frequency of GATA3+CD4+ Th2 and CD4+RORγt+ Th17 cells in the lungs of the allergic mice.Conclusion: Dietary intervention using GOS may be a novel way to further improve the efficacy of anti-inflammatory drug therapy in allergic asthma by lowering Th2 driving mediators and mast cell degranulation.

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“…Asthma has dramatically increased in incidence over the last decade, currently affecting 235 million people worldwide . According to epidemiological surveys, a cold environmental stimulus is believed a ‘trigger’ exacerbating existing asthma symptoms, or may directly trigger asthma .…”

Section: Introductionmentioning

confidence: 99%

“…Asthma has dramatically increased in incidence over the last decade, currently affecting 235 million people worldwide. [5][6][7] According to epidemiological surveys, a cold environmental stimulus is believed a 'trigger' exacerbating existing asthma symptoms, 8 or may directly trigger asthma. 9 Hyrkäs et al 10 surveyed 1623 young subjects and found that existing asthma increased the risks of all cold-weather related respiratory symptoms.…”

Section: Introductionmentioning

confidence: 99%

Repeated exposure to temperature variation exacerbates airway inflammation through TRPA1 in a mouse model of asthma

Kang

Chen

et al. 2018

Respirology

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Background and objective Studies from epidemiology suggest that ambient temperature is one of the underlying triggers and potential causes of asthma. The aim of this study was to examine the impact and the molecular mechanism of temperature‐invoked airway inflammation using an experimental model of asthma in BALB/c mice. Methods Mice were exposed to different temperature conditions (steady 26°C, 26°C/18°C cycle, 26°C/10°C cycle) and received sensitization and challenge of ovalbumin (OVA) during a 21‐day period. HC030031, a selective transient receptor potential A1 (TRPA1) channel blocker, was used to investigate the underlying mechanism of TRPA1 in ‘asthmatic’ airways. After the final OVA challenge, in vivo lung function was measured, and bronchoalveolar lavage fluid (BALF) and pulmonary inflammation were assessed. Results The temperature variations, especially the largest temperature difference (16°C), exacerbated airway inflammation in OVA‐induced mice, increasing the levels of serum total‐IgE (immunoglobulin E) and IgG1, inflammatory cells and cytokines in BALF. Analysis of histopathological changes and lung function verified that repeated exposure to very cold and changed temperatures aggravated airway hyperresponsiveness (AHR). Significant upregulation of TRPA1 expression was revealed by immunohistochemistry in the presence of the largest temperature variation (26°C/10°C cycle), while administration of HC030031 successfully inhibited TRPA1 expression, thus attenuating the asthma‐like pathological features. Conclusion Repeated exposure to temperature variation exacerbated experimental ‘asthma’ and TRPA1 mediated this temperature‐dependent inflammatory effect.

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Year in review 2017: Chronic obstructive pulmonary disease and asthma

Cited by 7 publications

References 81 publications

Phosphodiesterase-4 Inhibitors for the Treatment of Inflammatory Diseases

Phosphodiesterase-4 Inhibitors for the Treatment of Inflammatory Diseases

The Combination Therapy of Dietary Galacto-Oligosaccharides With Budesonide Reduces Pulmonary Th2 Driving Mediators and Mast Cell Degranulation in a Murine Model of House Dust Mite Induced Asthma

Repeated exposure to temperature variation exacerbates airway inflammation through TRPA1 in a mouse model of asthma

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