Evidence of a Role of Tumor Necrosis Factor α in Refractory Asthma
Patients with severe asthma are distinct from patients with milder forms of the disease. Peripheral-blood monocytes from patients with severe asthma were shown to have enhanced expression of markers associated with tumor necrosis factor α (TNF-α). In a pilot, placebo-controlled, crossover study, the...
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| Published in | The New England journal of medicine Vol. 354; no. 7; pp. 697 - 708 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Massachusetts Medical Society
16.02.2006
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0028-4793 1533-4406 1533-4406 |
| DOI | 10.1056/NEJMoa050580 |
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| Abstract | Patients with severe asthma are distinct from patients with milder forms of the disease. Peripheral-blood monocytes from patients with severe asthma were shown to have enhanced expression of markers associated with tumor necrosis factor α (TNF-α). In a pilot, placebo-controlled, crossover study, the TNF-α receptor–binding agent etanercept improved airway responsiveness and asthma-related quality of life. TNF-α may have a role in refractory asthma.
In a pilot study, the TNF-α receptor–binding agent etanercept improved airway responsiveness and asthma-related quality of life. TNF-α may have a role in refractory asthma.
The rates of death and complications are high among patients with refractory asthma and account for a disproportionate amount of the health resource burden attributed to asthma.
1
Treatment options are limited for these patients. The airway abnormality in refractory asthma differs from that in mild-to-moderate asthma in having a more heterogeneous pattern of inflammatory response,
2
with greater involvement of neutrophils
3
and the distal lung
4
and increased airway remodeling.
5
Tumor necrosis factor α (TNF-α) is a pleiotropic inflammatory cytokine expressed in increased amounts by mast cells
6
and present in increased concentrations in bronchoalveolar fluid from the airways of patients with asthma. . . . |
|---|---|
| AbstractList | Background The development of tumor necrosis factor alpha (TNF- alpha ) antagonists has made it feasible to investigate the role of this cytokine in refractory asthma. Methods We measured markers of TNF- alpha activity on peripheral-blood monocytes in 10 patients with refractory asthma, 10 patients with mild-to-moderate asthma, and 10 control subjects. We also investigated the effects of treatment with the soluble TNF- alpha receptor etanercept (25 mg twice weekly) in the patients with refractory asthma in a placebo-controlled, double-blind, crossover pilot study. Results As compared with patients with mild-to-moderate asthma and controls, patients with refractory asthma had increased expression of membrane-bound TNF- alpha , TNF- alpha receptor 1, and TNF- alpha -converting enzyme by peripheral-blood monocytes. In the clinical trial, as compared with placebo, 10 weeks of treatment with etanercept was associated with a significant increase in the concentration of methacholine required to provoke a 20 percent decrease in the forced expiratory volume in one second (FEV sub(1)) (mean difference in doubling concentration changes between etanercept and placebo, 3.5; 95 percent confidence interval, 0.07 to 7.0; P=0.05), an improvement in the asthma-related quality-of-life score (by 0.85 point; 95 percent confidence interval, 0.16 to 1.54 on a 7-point scale; P=0.02), and a 0.32-liter increase in post-bronchodilator FEV sub(1) (95 percent confidence interval, 0.08 to 0.55; P=0.01). Conclusions Patients with refractory asthma have evidence of up-regulation of the TNF- alpha axis. Patients with severe asthma are distinct from patients with milder forms of the disease. Peripheral-blood monocytes from patients with severe asthma were shown to have enhanced expression of markers associated with tumor necrosis factor α (TNF-α). In a pilot, placebo-controlled, crossover study, the TNF-α receptor–binding agent etanercept improved airway responsiveness and asthma-related quality of life. TNF-α may have a role in refractory asthma. In a pilot study, the TNF-α receptor–binding agent etanercept improved airway responsiveness and asthma-related quality of life. TNF-α may have a role in refractory asthma. The rates of death and complications are high among patients with refractory asthma and account for a disproportionate amount of the health resource burden attributed to asthma. 1 Treatment options are limited for these patients. The airway abnormality in refractory asthma differs from that in mild-to-moderate asthma in having a more heterogeneous pattern of inflammatory response, 2 with greater involvement of neutrophils 3 and the distal lung 4 and increased airway remodeling. 5 Tumor necrosis factor α (TNF-α) is a pleiotropic inflammatory cytokine expressed in increased amounts by mast cells 6 and present in increased concentrations in bronchoalveolar fluid from the airways of patients with asthma. . . . The development of tumor necrosis factor alpha (TNF-alpha) antagonists has made it feasible to investigate the role of this cytokine in refractory asthma. We measured markers of TNF-alpha activity on peripheral-blood monocytes in 10 patients with refractory asthma, 10 patients with mild-to-moderate asthma, and 10 control subjects. We also investigated the effects of treatment with the soluble TNF-alpha receptor etanercept (25 mg twice weekly) in the patients with refractory asthma in a placebo-controlled, double-blind, crossover pilot study. As compared with patients with mild-to-moderate asthma and controls, patients with refractory asthma had increased expression of membrane-bound TNF-alpha, TNF-alpha receptor 1, and TNF-alpha-converting enzyme by peripheral-blood monocytes. In the clinical trial, as compared with placebo, 10 weeks of treatment with etanercept was associated with a significant increase in the concentration of methacholine required to provoke a 20 percent decrease in the forced expiratory volume in one second (FEV1) (mean difference in doubling concentration changes between etanercept and placebo, 3.5; 95 percent confidence interval, 0.07 to 7.0; P=0.05), an improvement in the asthma-related quality-of-life score (by 0.85 point; 95 percent confidence interval, 0.16 to 1.54 on a 7-point scale; P=0.02), and a 0.32-liter increase in post-bronchodilator FEV1 (95 percent confidence interval, 0.08 to 0.55; P=0.01). Patients with refractory asthma have evidence of up-regulation of the TNF-alpha axis. (ClinicalTrials.gov number, NCT00276029.). The development of tumor necrosis factor alpha (TNF-alpha) antagonists has made it feasible to investigate the role of this cytokine in refractory asthma.BACKGROUNDThe development of tumor necrosis factor alpha (TNF-alpha) antagonists has made it feasible to investigate the role of this cytokine in refractory asthma.We measured markers of TNF-alpha activity on peripheral-blood monocytes in 10 patients with refractory asthma, 10 patients with mild-to-moderate asthma, and 10 control subjects. We also investigated the effects of treatment with the soluble TNF-alpha receptor etanercept (25 mg twice weekly) in the patients with refractory asthma in a placebo-controlled, double-blind, crossover pilot study.METHODSWe measured markers of TNF-alpha activity on peripheral-blood monocytes in 10 patients with refractory asthma, 10 patients with mild-to-moderate asthma, and 10 control subjects. We also investigated the effects of treatment with the soluble TNF-alpha receptor etanercept (25 mg twice weekly) in the patients with refractory asthma in a placebo-controlled, double-blind, crossover pilot study.As compared with patients with mild-to-moderate asthma and controls, patients with refractory asthma had increased expression of membrane-bound TNF-alpha, TNF-alpha receptor 1, and TNF-alpha-converting enzyme by peripheral-blood monocytes. In the clinical trial, as compared with placebo, 10 weeks of treatment with etanercept was associated with a significant increase in the concentration of methacholine required to provoke a 20 percent decrease in the forced expiratory volume in one second (FEV1) (mean difference in doubling concentration changes between etanercept and placebo, 3.5; 95 percent confidence interval, 0.07 to 7.0; P=0.05), an improvement in the asthma-related quality-of-life score (by 0.85 point; 95 percent confidence interval, 0.16 to 1.54 on a 7-point scale; P=0.02), and a 0.32-liter increase in post-bronchodilator FEV1 (95 percent confidence interval, 0.08 to 0.55; P=0.01).RESULTSAs compared with patients with mild-to-moderate asthma and controls, patients with refractory asthma had increased expression of membrane-bound TNF-alpha, TNF-alpha receptor 1, and TNF-alpha-converting enzyme by peripheral-blood monocytes. In the clinical trial, as compared with placebo, 10 weeks of treatment with etanercept was associated with a significant increase in the concentration of methacholine required to provoke a 20 percent decrease in the forced expiratory volume in one second (FEV1) (mean difference in doubling concentration changes between etanercept and placebo, 3.5; 95 percent confidence interval, 0.07 to 7.0; P=0.05), an improvement in the asthma-related quality-of-life score (by 0.85 point; 95 percent confidence interval, 0.16 to 1.54 on a 7-point scale; P=0.02), and a 0.32-liter increase in post-bronchodilator FEV1 (95 percent confidence interval, 0.08 to 0.55; P=0.01).Patients with refractory asthma have evidence of up-regulation of the TNF-alpha axis. (ClinicalTrials.gov number, NCT00276029.).CONCLUSIONSPatients with refractory asthma have evidence of up-regulation of the TNF-alpha axis. (ClinicalTrials.gov number, NCT00276029.). |
| Author | Hargadon, Beverley Parker, Debbie Shelley, Maria Shaw, Dominick E Pavord, Ian D Green, Ruth H Berry, Mike A Bradding, Peter Wardlaw, Andrew J Brightling, Christopher E |
| Author_xml | – sequence: 1 givenname: Mike A surname: Berry fullname: Berry, Mike A – sequence: 2 givenname: Beverley surname: Hargadon fullname: Hargadon, Beverley – sequence: 3 givenname: Maria surname: Shelley fullname: Shelley, Maria – sequence: 4 givenname: Debbie surname: Parker fullname: Parker, Debbie – sequence: 5 givenname: Dominick E surname: Shaw fullname: Shaw, Dominick E – sequence: 6 givenname: Ruth H surname: Green fullname: Green, Ruth H – sequence: 7 givenname: Peter surname: Bradding fullname: Bradding, Peter – sequence: 8 givenname: Christopher E surname: Brightling fullname: Brightling, Christopher E – sequence: 9 givenname: Andrew J surname: Wardlaw fullname: Wardlaw, Andrew J – sequence: 10 givenname: Ian D surname: Pavord fullname: Pavord, Ian D |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16481637$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2006 Massachusetts Medical Society. All rights reserved. Copyright 2006 Massachusetts Medical Society. |
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| Snippet | Patients with severe asthma are distinct from patients with milder forms of the disease. Peripheral-blood monocytes from patients with severe asthma were shown... The development of tumor necrosis factor alpha (TNF-alpha) antagonists has made it feasible to investigate the role of this cytokine in refractory asthma. We... Background The development of tumor necrosis factor alpha (TNF- alpha ) antagonists has made it feasible to investigate the role of this cytokine in refractory... The development of tumor necrosis factor alpha (TNF-alpha) antagonists has made it feasible to investigate the role of this cytokine in refractory... |
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| SubjectTerms | ADAM Proteins - biosynthesis ADAM17 Protein Adolescent Adult Aged Asthma - drug therapy Asthma - metabolism Asthma - physiopathology Biomarkers - metabolism Bronchial Hyperreactivity - drug therapy Bronchial Hyperreactivity - metabolism Case-Control Studies Cross-Over Studies Double-Blind Method Etanercept Female Forced Expiratory Volume - drug effects Humans Immunoglobulin G - therapeutic use Immunologic Factors - therapeutic use Male Methacholine Chloride Middle Aged Monocytes - metabolism Pilot Projects Receptors, Tumor Necrosis Factor - therapeutic use Receptors, Tumor Necrosis Factor, Type I - biosynthesis Treatment Outcome Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - metabolism Up-Regulation |
| Title | Evidence of a Role of Tumor Necrosis Factor α in Refractory Asthma |
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