1406 results found
Kole TM, Vanden Berghe E, Kraft M, et al., 2022, Predictors and associations of the persistent airflow limitation phenotype in asthma: a post-hoc analysis of the ATLANTIS study., The Lancet Respiratory Medicine, ISSN: 2213-2600
BACKGROUND: Persistent airflow limitation (PAL) occurs in a subset of patients with asthma. Previous studies on PAL in asthma have included relatively small populations, mostly restricted to severe asthma, or have no included longitudinal data. The aim of this post-hoc analysis was to investigate the determinants, clinical implications, and outcome of PAL in patients with asthma who were included in the ATLANTIS study. METHODS: In this post-hoc analysis of the ATLANTIS study, we assessed the prevalence, clinical characteristics, and implications of PAL across the full range of asthma severity. The study population included patients aged 18-65 years who had been diagnosed with asthma at least 6 months before inclusion. We defined PAL as a post-bronchodilator FEV1/forced vital capacity (FVC) of less than the lower limit of normal at recruitment. Asthma severity was defined according to the Global Initiative for Asthma. We used Mann-Whitney U test, t test, or χ2 test to analyse differences in baseline characteristics between patients with and without PAL. Logistic regression was used for multivariable analysis of the associations between PAL and baseline data. Cox regression was used to analyse risk of exacerbation in relation to PAL, and a linear mixed-effects model was used to analyse change in FEV1 over time in patients with versus patients without PAL. Results were validated in the U-BIOPRED cohort. FINDINGS: Between June 30, 2014 and March 3, 2017, 773 patients were enrolled in the ATLANTIS study of whom 760 (98%) had post-bronchodilator FEV1/FVC data available. Of the included patients with available data, mean age was 44 years (SD 13), 441 (58%) of 760 were women, 578 (76%) were never-smokers, and 248 (33%) had PAL. PAL was not only present in patients with severe asthma, but also in 21 (16%) of 133 patients with GINA step 1 and 24 (29%) of 83 patients with GINA step 2. PAL was independently associated with older age at baseline (46 years in PAL group vs 43
Lakhdar R, Mumby S, Abubakar-Waziri H, et al., 2022, Lung toxicity of particulates and gaseous pollutants using ex-vivo airway epithelial cell culture systems, ENVIRONMENTAL POLLUTION, Vol: 305, ISSN: 0269-7491
Marshall D, Al Omari O, Goodall R, et al., 2022, Trends in prevalence, mortality, and disability-adjusted life-years relating to Chronic Obstructive Pulmonary Disease in Europe: 2001-2019, BMC Pulmonary Medicine, ISSN: 1471-2466
Introduction:Chronic Obstructive Pulmonary Disease (COPD) is associated with significant mortality and well-defined etiological factors. Previous reports indicate that mortality from COPD is falling worldwide. This study aims to assess the burden of COPD using prevalence, mortality, and disability-adjusted life years (DALYs) between 2001-2019 in 28 European countries (the European Union and the United Kingdom).Methods: We extracted COPD data from the Global Burden of Disease database based on the International Classification of Diseases versions 10 (J41,42,43,44, and 47). Age-standardised prevalence rates (ASPRs), age-standardised mortality rates (ASMRs), and DALYs were analysed for European countries by sex for each year (2001-2019) and reported per 100,000 population. We used Joinpoint regression analysis to quantify changing trends in the burden of COPD.Results:In 2019, the median ASPR across Europe was 3230/100,000 for males and 2202/100,000 for females. Between 2001 and 2019, the median percentage change in ASPR was -9.7% for males and 4.3% for females. 23/28 countries demonstrated a decrease in ASPRs in males, and 11/28 demonstrated a decrease in females. The median percentage change in ASMR between 2001-2019 was -27.5% for males and -10.4% for females. 25/28 and 19/28 countries demonstrated a decrease in ASMR in males and females, respectively.Conclusion:In the EU between 2001 and 2019 COPD prevalence has overall increased in females but continues to decrease in males and in some countries, female prevalence now exceeds that of males. COPD mortality in the EU has decreased overall between 2001 and 2019; however, this decrease is not universal, particularly in females, and therefore remains a substantial source of amenable mortality. Funding:DCM is supported by an NIHR Academic Clinical Fellowship acknowledges support from the National Institute for Health Research (NIHR) Imperial Biomedical Research Centre. KFC is a Senior Investigator of the National Institu
Lo C-Y, Wang C-H, Wang C-W, et al., 2022, Increased Interleukin-17 and Glucocorticoid Receptor-beta Expression in Interstitial Lung Diseases and Corticosteroid Insensitivity, FRONTIERS IN IMMUNOLOGY, Vol: 13, ISSN: 1664-3224
Liu G, Jarnicki AG, Paudel KR, et al., 2022, Adverse roles of mast cell chymase-1 in chronic obstructive pulmonary disease., Eur Respir J
BACKGROUND: COPD is the third leading cause of death worldwide. Cigarette smoke (CS)-induced chronic inflammation inducing airway remodelling, emphysema and impaired lung function is the primary cause. Effective therapies are urgently needed. Human chymase-1 (hCMA1) and it's ortholog mCMA1/mouse mast cell (MC) protease-5 (mMCP5) are exocytosed from activated MCs and have adverse roles in numerous disorders, but their role in COPD is unknown. METHODS: We evaluated hCMA1 levels in lung tissues of COPD patients. We used mmcp5-deficient (-/-) mice to evaluate this proteases' role and potential for therapeutic targeting in CS-induced experimental COPD. We also used ex vivo/in vitro studies to define mechanisms. RESULTS: The levels of hCMA1 mRNA and CMA1+ MCs were increased in lung tissues from severe compared to early/mild COPD patients, non-COPD smokers and healthy controls. Degranulated MC numbers and mMCP5 protein were increased in lung tissues of wild-type (WT) mice with experimental COPD. mmcp5 -/- mice were protected against CS-induced inflammation and macrophage accumulation, airway remodelling, emphysema and impaired lung function in experimental COPD. CS extract challenge of co-cultures of MCs from WT but not mmcp5 -/- mice with WT lung macrophages increased in TNF-α release. It also caused the release of CMA1 from human MCs, and recombinant hCMA-1 induced TNF-α release from human macrophages. Treatment with CMA1 inhibitor potently suppressed these hallmark features of experimental COPD. CONCLUSION: CMA1/mMCP5 promotes the pathogenesis of COPD, in part, by inducing TNF-α expression and release from lung macrophages. Inhibiting hCMA1 may be a novel treatment for COPD.
Liu Z, Li Y-H, Cui Z-Y, et al., 2022, Prevalence of tobacco dependence and associated factors in China: Findings from nationwide China Health Literacy Survey during 2018-19, LANCET REGIONAL HEALTH-WESTERN PACIFIC, Vol: 24
Huang K, Gu X, Yang T, et al., 2022, Prevalence and burden of chronic cough in China: a national cross-sectional study., ERJ Open Res, Vol: 8, ISSN: 2312-0541
Background: Chronic cough is a common complaint, but there are no population-based data on its burden in China. We determined the prevalence of chronic cough and its impact on health status in adults stratified by sex, age and the diagnosis of COPD or the presence of small airway dysfunction (SAD). Methods: A representative sample of 57 779 Chinese adults aged 20 years or older was recruited and pulmonary function test was measured. Chronic cough was defined as cough lasting for >3 months in each year. Quality of life was assessed by the 12-item Short Form Health Survey (SF-12), and self-reported history of hospital visits was recorded. Results: Chronic cough was found in 3.6% (95% CI 3.1-4.1) of Chinese adults, 2.4% (95% CI 1.9-3.1) of those aged 20-49 years and 6.0% (95% CI 5.3-6.8) of those aged 50 years or older. Individuals with chronic cough had an impaired physical component summary (PCS) score of the SF-12 (p<0.0001) and more emergency visits (p=0.0042) and hospital admissions (p=0.0002). Furthermore, the impact of chronic cough on PCS score was more significant in those aged 50 years or older, or with COPD (p=0.0018 or 0.0002, respectively), with the impact on hospital admission being more significant in those with COPD or with SAD (p=0.0026 or 0.0065, respectively). Conclusions: Chronic cough is prevalent in China and is associated with a poorer health status, especially in individuals aged 50 years or older and those with the diagnosis of COPD or SAD.
Frankenberg Garcia J, Rogers AV, Mak JCW, et al., 2022, Mitochondrial Transfer Regulates Bioenergetics in Healthy and COPD Airway Smooth Muscle., Am J Respir Cell Mol Biol
Mitochondrial dysfunction has been reported in chronic obstructive pulmonary disease (COPD). Transfer of mitochondria from mesenchymal stem cells to airway smooth muscle cells (ASMCs) can attenuate oxidative stress-induced mitochondrial damage. It is not known whether mitochondrial transfer occurs between structural cells in the lungs nor what role this may have in modulating bioenergetics and cellular function in healthy and COPD airways. Here, we show that ASMCs from both healthy ex-smoker and COPD subjects can exchange mitochondria, a process that happens, at least partly, via extracellular vesicles. Exposure to cigarette smoke induces mitochondrial dysfunction and leads to an increase in the donation of mitochondria by ASMCs, suggesting the latter may be a stress response mechanism. Healthy ex-smoker ASMCs that receive mitochondria show an increase in mitochondrial biogenesis and respiration and a reduction in cell proliferation, irrespective of whether the mitochondria are transferred from healthy ex-smoker or COPD ASMCs. Our data indicate that mitochondrial transfer between structural cells is a homeostatic mechanism for the regulation of bioenergetics and cellular function within the airways and may represent an endogenous mechanism for reversing the functional consequences of mitochondrial dysfunction in diseases such as COPD.
Tran HM, Chen T-T, Lu Y-H, et al., 2022, Climate-mediated air pollution associated with COPD severity., Sci Total Environ, Vol: 843
Air pollution has been reported to be associated with chronic obstructive pulmonary disease (COPD). Our study aim was to examine the mediating effects of air pollution on climate-associated health outcomes of COPD patients. A cross-sectional study of 117 COPD patients was conducted in a hospital in Taiwan. We measured the lung function, 6-min walking distance, oxygen desaturation, white blood cell count, and percent emphysema (low attenuation area, LAA) and linked these to 0-1-, 0-3-, and 0-5-year lags of individual-level exposure to relative humidity (RH), temperature, and air pollution. Linear regression models were conducted to examine associations of temperature, RH, and air pollution with severity of health outcomes. A mediation analysis was conducted to examine the mediating effects of air pollution on the associations of RH and temperature with health outcomes. We observed that a 1 % increase in the RH was associated with increases in forced expiratory volume in 1 s (FEV1), eosinophils, and lymphocytes, and a decrease in the total-lobe LAA. A 1 °C increase in temperature was associated with decreases in oxygen desaturation, and right-, left-, and upper-lobe LAA values. Also, a 1 μg/m3 increase in PM2.5 was associated with a decrease in the FEV1 and an increase in oxygen desaturation. A 1 μg/m3 increases in PM10 and PM2.5 was associated with increases in the total-, right-, left, upper-, and lower-lobe (PM2.5 only) LAA. A one part per billion increase in NO2 was associated with a decrease in the FEV1 and an increase in the upper-lobe LAA. Next, we found that NO2 fully mediated the association between RH and FEV1. We found PM2.5 fully mediated associations of temperature with oxygen saturation and total-, right-, left-, and upper-lobe LAA. In conclusion, climate-mediated air pollution increased the risk of decreasing FEV1 and oxygen saturation and increasing emphysema severity among COPD patients. Climate change-related air pollution is an important p
Sanchez-Ovando S, Pavlidis S, Kermani NZ, et al., 2022, Pathways linked to unresolved inflammation and airway remodelling characterize the transcriptome in two independent severe asthma cohorts, RESPIROLOGY, ISSN: 1323-7799
Michaeloudes C, Abubakar-Waziri H, Lakhdar R, et al., 2022, Molecular mechanisms of oxidative stress in asthma, Molecular Aspects of Medicine, Vol: 85, ISSN: 0098-2997
The lungs are exposed to reactive oxygen species oxygen (ROS) produced as a result of inhalation of oxygen, as well as smoke and other air pollutants. Cell metabolism and the NADPH oxidases (Nox) generate low levels of intracellular ROS that act as signal transduction mediators by inducing oxidative modifications of histones, enzymes and transcription factors. Redox signalling is also regulated by localised production and sensing of ROS in mitochondria, the endoplasmic reticulum (ER) and inside the nucleus. Intracellular ROS are maintained at low levels through the action of a battery of enzymatic and non-enzymatic antioxidants. Asthma is a heterogeneous airway inflammatory disease with different immune endotypes; these include atopic or non-atopic Th2 type immune response associated with eosinophilia, or a non-Th2 response associated with neutrophilia. Airway remodelling and hyperresponsiveness accompany the inflammatory response in asthma. Over-production of ROS resulting from infiltrating immune cells, particularly eosinophils and neutrophils, and a concomitant impairment of antioxidant responses lead to development of oxidative stress in asthma. Oxidative stress is augmented in severe asthma and during exacerbations, as well as by air pollution and obesity, and causes oxidative damage of tissues promoting airway inflammation and hyperresponsiveness. Furthermore, deregulated Nox activity, mitochondrial dysfunction, ER stress and/or oxidative DNA damage, resulting from exposure to irritants, inflammatory mediators or obesity, may lead to redox-dependent changes in cell signalling. ROS play a central role in airway epithelium-mediated sensing, development of innate and adaptive immune responses, and airway remodelling and hyperresponsiveness. Nonetheless, antioxidant compounds have proven clinically ineffective as therapeutic agents for asthma, partly due to issues with stability and in vivo metabolism of these compounds. The compartmentalised nature of ROS product
Reinke SN, Naz S, Chaleckis R, et al., 2022, Urinary metabotype of severe asthma evidences decreased carnitine metabolism independent of oral corticosteroid treatment in the U-BIOPRED study., Eur Respir J, Vol: 59
INTRODUCTION: Asthma is a heterogeneous disease with poorly defined phenotypes. Patients with severe asthma often receive multiple treatments including oral corticosteroids (OCS). Treatment may modify the observed metabotype, rendering it challenging to investigate underlying disease mechanisms. Here, we aimed to identify dysregulated metabolic processes in relation to asthma severity and medication. METHODS: Baseline urine was collected prospectively from healthy participants (n=100), patients with mild-to-moderate asthma (n=87) and patients with severe asthma (n=418) in the cross-sectional U-BIOPRED cohort; 12-18-month longitudinal samples were collected from patients with severe asthma (n=305). Metabolomics data were acquired using high-resolution mass spectrometry and analysed using univariate and multivariate methods. RESULTS: A total of 90 metabolites were identified, with 40 significantly altered (p<0.05, false discovery rate <0.05) in severe asthma and 23 by OCS use. Multivariate modelling showed that observed metabotypes in healthy participants and patients with mild-to-moderate asthma differed significantly from those in patients with severe asthma (p=2.6×10-20), OCS-treated asthmatic patients differed significantly from non-treated patients (p=9.5×10-4), and longitudinal metabotypes demonstrated temporal stability. Carnitine levels evidenced the strongest OCS-independent decrease in severe asthma. Reduced carnitine levels were associated with mitochondrial dysfunction via decreases in pathway enrichment scores of fatty acid metabolism and reduced expression of the carnitine transporter SLC22A5 in sputum and bronchial brushings. CONCLUSIONS: This is the first large-scale study to delineate disease- and OCS-associated metabolic differences in asthma. The widespread associations with different therapies upon the observed metabotypes demonstrate the need to evaluate potential modulating effects on a treatment- and metabolite-specific basis.
Chung KF, Dixey P, Abubakar-Waziri H, et al., 2022, Characteristics, phenotypes, mechanisms and management of severe asthma., Chin Med J (Engl)
ABSTRACT: Severe asthma is "asthma which requires treatment with high dose inhaled corticosteroids (ICS) plus a second controller (and/or systemic corticosteroids) to prevent it from becoming 'uncontrolled' or which remains 'uncontrolled' despite this therapy." The state of control was defined by symptoms, exacerbations and the degree of airflow obstruction. Therefore, for the diagnosis of severe asthma, it is important to have evidence for a diagnosis of asthma with an assessment of its severity, followed by a review of comorbidities, risk factors, triggers and an assessment of whether treatment is commensurate with severity, whether the prescribed treatments have been adhered to and whether inhaled therapy has been properly administered. Phenotyping of severe asthma has been introduced with the definition of a severe eosinophilic asthma phenotype characterized by recurrent exacerbations despite being on high dose ICS and sometimes oral corticosteroids, with a high blood eosinophil count and a raised level of nitric oxide in exhaled breath. This phenotype has been associated with a Type-2 (T2) inflammatory profile with expression of interleukin (IL)-4, IL-5, and IL-13. Molecular phenotyping has also revealed non-T2 inflammatory phenotypes such as Type-1 or Type-17 driven phenotypes. Antibody treatments targeted at the T2 targets such as anti-IL5, anti-IL5Rα, and anti-IL4Rα antibodies are now available for treating severe eosinophilic asthma, in addition to anti-immunoglobulin E antibody for severe allergic asthma. No targeted treatments are currently available for non-T2 inflammatory phenotypes. Long-term azithromycin and bronchial thermoplasty may be considered. The future lies with molecular phenotyping of the airway inflammatory process to refine asthma endotypes for precision medicine.
Li C, Zhang H, Wei L, et al., 2022, Role of TRPA1/TRPV1 in acute ozone exposure induced murine model of airway inflammation and bronchial hyperresponsiveness, Journal of Thoracic Disease, ISSN: 2072-1439
Background: Transient receptor potential (TRP) ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) mediatethe development of lung injury and inflammation. This study investigated the role and mechanism of theTRPA1/TRPV1 pathway in airway inflammation and bronchial hyperresponsiveness (BHR) induced byacute ozone exposure.Methods: C57BL/6 mice (8–10 weeks) were intraperitoneally injected with phosphate buffered saline(PBS), A967079 (TRPA1 inhibitor) or AMG9810 (TRPV1 inhibitor) 1 h before or after ozone exposure(2.5 ppm, 3 h). BHR, cell counts in bronchoalveolar lavage (BAL) fluid, oxidative stress biomarkers,inflammatory cytokines, TRPA1 and TPRV1 protein levels, mitochondrial dynamics- and mitophagy-relatedprotein levels, and activities of mitochondrial respiratory chain (MRC) in lung were measured.Results: The preventive treatment effect was similar to the therapeutic treatment effect. Both A967079 andAMG9810 intervention suppressed BHR, inflammatory cytokines, total BAL fluid cells, malondialdehyde(MDA) levels and inflammatory cytokines mRNA including Substance P (SP), Keratinocyte-DerivedChemokine (KC), interleukin18 (IL-18) and chemokine (C-X-C motif) ligand 8 (CXCL8) expression, andenhanced reduced glutathione (GSH)/oxidized glutathione (GSSG) levels compared with ozone-exposedmice. A967079 and AMG9810 intervention inhibited dynamin-related protein (DRP1), mitochondrial fissionfactor (MFF), Parkinson protein 2 E3 ubiquitin protein ligase (PARK2) and Sequestosome 1 (SQSTM1)/p62expression, increased Optic atrophy 1 (OPA1), mitofusin 2 (MFN2) and PTEN-induced putative kinase 1(PINK1) expression, and up-regulated the activities of MRC complex III and V in lung tissue.Conclusions: The results show that both TRPA1 and TRPV1 pathways are involved in acute ozoneexposure-induced airway inflammation and BHR and influence oxidative stress, mitochondrial qualitycontrol and MRC activity, which could be a potential target for clinical therapy of respiritory disease
Yeh L-Y, Fang Y-T, Lee H-S, et al., 2022, A Potent Histone Deacetylase Inhibitor MPT0E028 Mitigates Emphysema Severity via Components of the Hippo Signaling Pathway in an Emphysematous Mouse Model, FRONTIERS IN MEDICINE, Vol: 9
Wang C-H, Lo C-Y, Huang H-Y, et al., 2022, Oxygen Desaturation Is Associated With Fibrocyte Activation via Epidermal Growth Factor Receptor/Hypoxia- Inducible Factor-1a Axis in Chronic Obstructive Pulmonary Disease, FRONTIERS IN IMMUNOLOGY, Vol: 13, ISSN: 1664-3224
Deng SJ, Wang J, Liu L, et al., 2022, Chronic cough in asthma is associated with increased airway inflammation, more comorbidities, and worse clinical outcomes, ALLERGY AND ASTHMA PROCEEDINGS, Vol: 43, Pages: 209-219, ISSN: 1088-5412
Masfufa IW, Chung KF, Adcock I, 2022, Clinical characteristic of severe asthma patients with JAK-STAT pathway activation, Publisher: ELSEVIER, Pages: S32-S32, ISSN: 0009-8981
Kang YR, Oh J-Y, Lee J-H, et al., 2022, Long-COVID severe refractory cough: discussion of a case with 6-week longitudinal cough characterization, ASIA PACIFIC ALLERGY, Vol: 12, ISSN: 2233-8276
Chen R, Michaeloudes C, Liang Y, et al., 2022, ORMDL3 regulates cigarette smoke-induced endoplasmic reticulum stress in airway smooth muscle cells, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 149, Pages: 1445-+, ISSN: 0091-6749
Lee K-Y, Wu S-M, Kou H-Y, et al., 2022, Association of air pollution exposure with exercise-induced oxygen desaturation in COPD, RESPIRATORY RESEARCH, Vol: 23
Liu W-T, Wang Y-H, Chang L-T, et al., 2022, The impacts of ambient relative humidity and temperature on supine position-related obstructive sleep apnea in adults, ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH, ISSN: 0944-1344
Tiotiu A, Badi Y, Kermani NZ, et al., 2022, Association of Differential Mast Cell Activation with Granulocytic Inflammation in Severe Asthma, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 205, Pages: 397-+, ISSN: 1073-449X
Zhang Q, Fu X, Wang C, et al., 2022, Severe eosinophilic asthma in Chinese C-BIOPRED asthma cohort, CLINICAL AND TRANSLATIONAL MEDICINE, Vol: 12, ISSN: 2001-1326
Mikus MS, Kolmert J, Andersson L, et al., 2022, Plasma proteins elevated in severe asthma despite oral steroid use and unrelated to Type-2 inflammation, EUROPEAN RESPIRATORY JOURNAL, Vol: 59, ISSN: 0903-1936
Lai K, Zhan W, Wu F, et al., 2022, Clinical and Inflammatory Characteristics of the Chinese APAC Cough Variant Asthma Cohort, FRONTIERS IN MEDICINE, Vol: 8
Huang H-Y, Chung F-T, Lin C-Y, et al., 2022, Influence of Comorbidities and Airway Clearance on Mortality and Outcomes of Patients With Severe Bronchiectasis Exacerbations in Taiwan, FRONTIERS IN MEDICINE, Vol: 8
Chang J-H, Lee Y-L, Laiman V, et al., 2022, Air pollution-regulated E-cadherin mediates contact inhibition of proliferation via the hippo signaling pathways in emphysema, CHEMICO-BIOLOGICAL INTERACTIONS, Vol: 351, ISSN: 0009-2797
Badi Y, Pavel AB, Pavlidis S, et al., 2022, Mapping atopic dermatitis and anti–IL-22 response signatures to type 2–low severe neutrophilic asthma, Journal of Allergy and Clinical Immunology, Vol: 149, Pages: 89-101, ISSN: 0091-6749
Background:Transcriptomic changes in patients who respond clinically to biological therapies may identify responses in other tissues or diseases.Objective:We sought to determine whether a disease signature identified in atopic dermatitis (AD) is seen in adults with severe asthma and whether a transcriptomic signature for patients with AD who respond clinically to anti–IL-22 (fezakinumab [FZ]) is enriched in severe asthma.Methods:An AD disease signature was obtained from analysis of differentially expressed genes between AD lesional and nonlesional skin biopsies. Differentially expressed genes from lesional skin from therapeutic superresponders before and after 12 weeks of FZ treatment defined the FZ-response signature. Gene set variation analysis was used to produce enrichment scores of AD and FZ-response signatures in the Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes asthma cohort.Results:The AD disease signature (112 upregulated genes) encompassing inflammatory, T-cell, TH2, and TH17/TH22 pathways was enriched in the blood and sputum of patients with asthma with increasing severity. Patients with asthma with sputum neutrophilia and mixed granulocyte phenotypes were the most enriched (P < .05). The FZ-response signature (296 downregulated genes) was enriched in asthmatic blood (P < .05) and particularly in neutrophilic and mixed granulocytic sputum (P < .05). These data were confirmed in sputum of the Airway Disease Endotyping for Personalized Therapeutics cohort. IL-22 mRNA across tissues did not correlate with FZ-response enrichment scores, but this response signature correlated with TH22/IL-22 pathways.Conclusions:The FZ-response signature in AD identifies severe neutrophilic asthmatic patients as potential responders to FZ therapy. This approach will help identify patients for future asthma clinical trials of drugs used successfully in other chronic diseases.
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.