Refractory airway type 2 inflammation in a large subgroup of asthmatic patients treated with inhaled corticosteroids
Airway type 2 inflammation is usually corticosteroid sensitive, but the role of type 2 inflammation as a mechanism of asthma in patients receiving high-dose inhaled corticosteroids (ICSs) is uncertain. We sought to determine whether airway type 2 inflammation persists in patients treated with ICSs a...
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| Published in | Journal of allergy and clinical immunology Vol. 143; no. 1; pp. 104 - 113.e14 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.01.2019
Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Airway type 2 inflammation is usually corticosteroid sensitive, but the role of type 2 inflammation as a mechanism of asthma in patients receiving high-dose inhaled corticosteroids (ICSs) is uncertain.
We sought to determine whether airway type 2 inflammation persists in patients treated with ICSs and to evaluate the clinical features of patients with steroid-resistant airway type 2 inflammation.
We used quantitative PCR to generate a composite metric of type 2 cytokine gene expression (type 2 gene mean [T2GM]) in induced sputum cells from healthy control subjects, patients with severe asthma receiving ICSs (n = 174), and patients with nonsevere asthma receiving ICSs (n = 85). We explored relationships between asthma outcomes and T2GM values and the utility of noninvasive biomarkers of airway T2GM.
Sputum cell T2GM values in asthmatic patients were significantly increased and remained high after treatment with intramuscular triamcinolone. We used the median T2GM value as a cutoff to classify steroid-treated type 2–low and steroid-resistant type 2–high (srT2-high) subgroups. Compared with patients with steroid-treated type 2–low asthma, those with srT2-high asthma were older and had more severe asthma. Blood eosinophil cell counts predicted srT2-high asthma when body mass index was less than 40 kg/m2 but not when it was 40 kg/m2 or greater, whereas blood IgE levels strongly predicted srT2-high asthma when age was less than 34 years but not when it was 34 years or greater.
Despite ICS therapy, many asthmatic patients have persistent airway type 2 inflammation (srT2-high asthma), and these patients are older and have more severe disease. Body weight and age modify the performance of blood-based biomarkers of airway type 2 inflammation. |
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| AbstractList | Airway type 2 inflammation is usually corticosteroid sensitive, but the role of type 2 inflammation as a mechanism of asthma in patients receiving high-dose inhaled corticosteroids (ICSs) is uncertain.
We sought to determine whether airway type 2 inflammation persists in patients treated with ICSs and to evaluate the clinical features of patients with steroid-resistant airway type 2 inflammation.
We used quantitative PCR to generate a composite metric of type 2 cytokine gene expression (type 2 gene mean [T2GM]) in induced sputum cells from healthy control subjects, patients with severe asthma receiving ICSs (n = 174), and patients with nonsevere asthma receiving ICSs (n = 85). We explored relationships between asthma outcomes and T2GM values and the utility of noninvasive biomarkers of airway T2GM.
Sputum cell T2GM values in asthmatic patients were significantly increased and remained high after treatment with intramuscular triamcinolone. We used the median T2GM value as a cutoff to classify steroid-treated type 2-low and steroid-resistant type 2-high (srT2-high) subgroups. Compared with patients with steroid-treated type 2-low asthma, those with srT2-high asthma were older and had more severe asthma. Blood eosinophil cell counts predicted srT2-high asthma when body mass index was less than 40 kg/m
but not when it was 40 kg/m
or greater, whereas blood IgE levels strongly predicted srT2-high asthma when age was less than 34 years but not when it was 34 years or greater.
Despite ICS therapy, many asthmatic patients have persistent airway type 2 inflammation (srT2-high asthma), and these patients are older and have more severe disease. Body weight and age modify the performance of blood-based biomarkers of airway type 2 inflammation. Airway type 2 inflammation is usually corticosteroid sensitive, but the role of type 2 inflammation as a mechanism of asthma in patients receiving high-dose inhaled corticosteroids (ICSs) is uncertain. We sought to determine whether airway type 2 inflammation persists in patients treated with ICSs and to evaluate the clinical features of patients with steroid-resistant airway type 2 inflammation. We used quantitative PCR to generate a composite metric of type 2 cytokine gene expression (type 2 gene mean [T2GM]) in induced sputum cells from healthy control subjects, patients with severe asthma receiving ICSs (n = 174), and patients with nonsevere asthma receiving ICSs (n = 85). We explored relationships between asthma outcomes and T2GM values and the utility of noninvasive biomarkers of airway T2GM. Sputum cell T2GM values in asthmatic patients were significantly increased and remained high after treatment with intramuscular triamcinolone. We used the median T2GM value as a cutoff to classify steroid-treated type 2–low and steroid-resistant type 2–high (srT2-high) subgroups. Compared with patients with steroid-treated type 2–low asthma, those with srT2-high asthma were older and had more severe asthma. Blood eosinophil cell counts predicted srT2-high asthma when body mass index was less than 40 kg/m2 but not when it was 40 kg/m2 or greater, whereas blood IgE levels strongly predicted srT2-high asthma when age was less than 34 years but not when it was 34 years or greater. Despite ICS therapy, many asthmatic patients have persistent airway type 2 inflammation (srT2-high asthma), and these patients are older and have more severe disease. Body weight and age modify the performance of blood-based biomarkers of airway type 2 inflammation. Airway type 2 inflammation is usually corticosteroid sensitive, but the role of type 2 inflammation as a mechanism of asthma in patients receiving high-dose inhaled corticosteroids (ICSs) is uncertain.BACKGROUNDAirway type 2 inflammation is usually corticosteroid sensitive, but the role of type 2 inflammation as a mechanism of asthma in patients receiving high-dose inhaled corticosteroids (ICSs) is uncertain.We sought to determine whether airway type 2 inflammation persists in patients treated with ICSs and to evaluate the clinical features of patients with steroid-resistant airway type 2 inflammation.OBJECTIVEWe sought to determine whether airway type 2 inflammation persists in patients treated with ICSs and to evaluate the clinical features of patients with steroid-resistant airway type 2 inflammation.We used quantitative PCR to generate a composite metric of type 2 cytokine gene expression (type 2 gene mean [T2GM]) in induced sputum cells from healthy control subjects, patients with severe asthma receiving ICSs (n = 174), and patients with nonsevere asthma receiving ICSs (n = 85). We explored relationships between asthma outcomes and T2GM values and the utility of noninvasive biomarkers of airway T2GM.METHODSWe used quantitative PCR to generate a composite metric of type 2 cytokine gene expression (type 2 gene mean [T2GM]) in induced sputum cells from healthy control subjects, patients with severe asthma receiving ICSs (n = 174), and patients with nonsevere asthma receiving ICSs (n = 85). We explored relationships between asthma outcomes and T2GM values and the utility of noninvasive biomarkers of airway T2GM.Sputum cell T2GM values in asthmatic patients were significantly increased and remained high after treatment with intramuscular triamcinolone. We used the median T2GM value as a cutoff to classify steroid-treated type 2-low and steroid-resistant type 2-high (srT2-high) subgroups. Compared with patients with steroid-treated type 2-low asthma, those with srT2-high asthma were older and had more severe asthma. Blood eosinophil cell counts predicted srT2-high asthma when body mass index was less than 40 kg/m2 but not when it was 40 kg/m2 or greater, whereas blood IgE levels strongly predicted srT2-high asthma when age was less than 34 years but not when it was 34 years or greater.RESULTSSputum cell T2GM values in asthmatic patients were significantly increased and remained high after treatment with intramuscular triamcinolone. We used the median T2GM value as a cutoff to classify steroid-treated type 2-low and steroid-resistant type 2-high (srT2-high) subgroups. Compared with patients with steroid-treated type 2-low asthma, those with srT2-high asthma were older and had more severe asthma. Blood eosinophil cell counts predicted srT2-high asthma when body mass index was less than 40 kg/m2 but not when it was 40 kg/m2 or greater, whereas blood IgE levels strongly predicted srT2-high asthma when age was less than 34 years but not when it was 34 years or greater.Despite ICS therapy, many asthmatic patients have persistent airway type 2 inflammation (srT2-high asthma), and these patients are older and have more severe disease. Body weight and age modify the performance of blood-based biomarkers of airway type 2 inflammation.CONCLUSIONDespite ICS therapy, many asthmatic patients have persistent airway type 2 inflammation (srT2-high asthma), and these patients are older and have more severe disease. Body weight and age modify the performance of blood-based biomarkers of airway type 2 inflammation. BackgroundAirway type 2 inflammation is usually corticosteroid sensitive, but the role of type 2 inflammation as a mechanism of asthma in patients receiving high-dose inhaled corticosteroids (ICSs) is uncertain.ObjectiveWe sought to determine whether airway type 2 inflammation persists in patients treated with ICSs and to evaluate the clinical features of patients with steroid-resistant airway type 2 inflammation.MethodsWe used quantitative PCR to generate a composite metric of type 2 cytokine gene expression (type 2 gene mean [T2GM]) in induced sputum cells from healthy control subjects, patients with severe asthma receiving ICSs (n = 174), and patients with nonsevere asthma receiving ICSs (n = 85). We explored relationships between asthma outcomes and T2GM values and the utility of noninvasive biomarkers of airway T2GM.ResultsSputum cell T2GM values in asthmatic patients were significantly increased and remained high after treatment with intramuscular triamcinolone. We used the median T2GM value as a cutoff to classify steroid-treated type 2–low and steroid-resistant type 2–high (srT2-high) subgroups. Compared with patients with steroid-treated type 2–low asthma, those with srT2-high asthma were older and had more severe asthma. Blood eosinophil cell counts predicted srT2-high asthma when body mass index was less than 40 kg/m2 but not when it was 40 kg/m2 or greater, whereas blood IgE levels strongly predicted srT2-high asthma when age was less than 34 years but not when it was 34 years or greater.ConclusionDespite ICS therapy, many asthmatic patients have persistent airway type 2 inflammation (srT2-high asthma), and these patients are older and have more severe disease. Body weight and age modify the performance of blood-based biomarkers of airway type 2 inflammation. |
| Author | Wenzel, Sally E. Fahy, John V. Castro, Mario Hastie, Annette T. Israel, Elliot Coverstone, Andrea M. Fajt, Merritt L. Kerr, Sheena Johansson, Mats W. Erzurum, Serpil C. Peters, Michael C. Bleecker, Eugene R. Woodruff, Prescott G. Jarjour, Nizar N. Phillips, Brenda R. Dunican, Eleanor M. Comhair, Suzy A. Mauger, David T. Levy, Bruce D. |
| AuthorAffiliation | f Department of Biomolecular Chemistry, University of Wisconsin School of Medicine, Madison a Division of Pulmonary and Critical Care Medicine, Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco b Pulmonary, Allergy and Critical Care Medicine Division, Department of Medicine, University of Pittsburgh School of Medicine j Center for Genomics and Personalized Medicine Research, School of Medicine, Wake Forest University, Winston-Salem e Department of Pathobiology, Cleveland Clinic Cleveland i Division of Pulmonary and Critical Care Medicine, Departments of Medicine and Pediatrics, Washington University, St Louis c Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston g Section of Pulmonary and Critical Care Medicine, University of Wisconsin School of Medicine, Madison h Division of Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Washingto |
| AuthorAffiliation_xml | – name: a Division of Pulmonary and Critical Care Medicine, Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco – name: c Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston – name: g Section of Pulmonary and Critical Care Medicine, University of Wisconsin School of Medicine, Madison – name: j Center for Genomics and Personalized Medicine Research, School of Medicine, Wake Forest University, Winston-Salem – name: d Division of Statistics and Bioinformatics, Department of Public Health Sciences, Pennsylvania State University, Hershey – name: i Division of Pulmonary and Critical Care Medicine, Departments of Medicine and Pediatrics, Washington University, St Louis – name: b Pulmonary, Allergy and Critical Care Medicine Division, Department of Medicine, University of Pittsburgh School of Medicine – name: f Department of Biomolecular Chemistry, University of Wisconsin School of Medicine, Madison – name: h Division of Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Washington University School of Medicine, St Louis – name: e Department of Pathobiology, Cleveland Clinic Cleveland |
| Author_xml | – sequence: 1 givenname: Michael C. orcidid: 0000-0003-1854-4447 surname: Peters fullname: Peters, Michael C. organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco, San Francisco, Calif – sequence: 2 givenname: Sheena surname: Kerr fullname: Kerr, Sheena organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco, San Francisco, Calif – sequence: 3 givenname: Eleanor M. surname: Dunican fullname: Dunican, Eleanor M. organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco, San Francisco, Calif – sequence: 4 givenname: Prescott G. surname: Woodruff fullname: Woodruff, Prescott G. organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco, San Francisco, Calif – sequence: 5 givenname: Merritt L. surname: Fajt fullname: Fajt, Merritt L. organization: Pulmonary, Allergy and Critical Care Medicine Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pa – sequence: 6 givenname: Bruce D. surname: Levy fullname: Levy, Bruce D. organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass – sequence: 7 givenname: Elliot surname: Israel fullname: Israel, Elliot organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass – sequence: 8 givenname: Brenda R. surname: Phillips fullname: Phillips, Brenda R. organization: Division of Statistics and Bioinformatics, Department of Public Health Sciences, Pennsylvania State University, Hershey, Pa – sequence: 9 givenname: David T. surname: Mauger fullname: Mauger, David T. organization: Division of Statistics and Bioinformatics, Department of Public Health Sciences, Pennsylvania State University, Hershey, Pa – sequence: 10 givenname: Suzy A. orcidid: 0000-0003-1918-9002 surname: Comhair fullname: Comhair, Suzy A. organization: Department of Pathobiology, Cleveland Clinic Cleveland, Cleveland, Ohio – sequence: 11 givenname: Serpil C. surname: Erzurum fullname: Erzurum, Serpil C. organization: Department of Pathobiology, Cleveland Clinic Cleveland, Cleveland, Ohio – sequence: 12 givenname: Mats W. orcidid: 0000-0001-5699-978X surname: Johansson fullname: Johansson, Mats W. organization: Department of Biomolecular Chemistry, University of Wisconsin School of Medicine, Madison, Wis – sequence: 13 givenname: Nizar N. surname: Jarjour fullname: Jarjour, Nizar N. organization: Section of Pulmonary and Critical Care Medicine, University of Wisconsin School of Medicine, Madison, Wis – sequence: 14 givenname: Andrea M. orcidid: 0000-0002-9666-4885 surname: Coverstone fullname: Coverstone, Andrea M. organization: Division of Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Washington University School of Medicine, St Louis, Mo – sequence: 15 givenname: Mario orcidid: 0000-0001-6328-8994 surname: Castro fullname: Castro, Mario organization: Division of Pulmonary and Critical Care Medicine, Departments of Medicine and Pediatrics, Washington University, St Louis, Mo – sequence: 16 givenname: Annette T. surname: Hastie fullname: Hastie, Annette T. organization: Center for Genomics and Personalized Medicine Research, School of Medicine, Wake Forest University, Winston-Salem, NC – sequence: 17 givenname: Eugene R. surname: Bleecker fullname: Bleecker, Eugene R. organization: Center for Genomics and Personalized Medicine Research, School of Medicine, Wake Forest University, Winston-Salem, NC – sequence: 18 givenname: Sally E. surname: Wenzel fullname: Wenzel, Sally E. organization: Pulmonary, Allergy and Critical Care Medicine Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pa – sequence: 19 givenname: John V. surname: Fahy fullname: Fahy, John V. email: John.Fahy@ucsf.edu organization: Division of Pulmonary and Critical Care Medicine, Department of Medicine and the Cardiovascular Research Institute, University of California San Francisco, San Francisco, Calif |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29524537$$D View this record in MEDLINE/PubMed |
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| Copyright | 2018 American Academy of Allergy, Asthma & Immunology Copyright © 2018 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved. Copyright Elsevier Limited Jan 2019 |
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| Keywords | steroid resistance Feno stT2-low T2GM biomarkers ROC SARP AUC CT RIN OLS ICS Severe asthma type 2 inflammation srT2-high BMI |
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| SubjectTerms | Administration, Inhalation Adrenal Cortex Hormones - administration & dosage Adult Age Asthma Asthma - blood Asthma - drug therapy Asthma - immunology Biomarkers Biomarkers - blood Blood levels Body mass index Body weight Corticosteroids Cytokines Cytokines - blood Cytokines - immunology Eosinophils - immunology Eosinophils - metabolism Eosinophils - pathology Family medical history Female Gene expression Gene Expression Regulation - drug effects Gene Expression Regulation - immunology Health care Humans Immunoglobulin E Immunoglobulin E - blood Immunoglobulin E - immunology Immunomodulators Inflammation Inflammation - blood Inflammation - immunology Leukocyte Count Leukocytes (eosinophilic) Longitudinal Studies Male Middle Aged Patients Respiratory tract Severe asthma Sputum steroid resistance Th2 Cells - immunology Th2 Cells - metabolism type 2 inflammation Values |
| Title | Refractory airway type 2 inflammation in a large subgroup of asthmatic patients treated with inhaled corticosteroids |
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