Similar colds in subjects with allergic asthma and nonatopic subjects after inoculation with rhinovirus-16
Rhinovirus infections are frequent causes of asthma exacerbations. This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes. Twenty subjects with mild persistent a...
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| Published in | Journal of allergy and clinical immunology Vol. 124; no. 2; pp. 245 - 252.e3 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.08.2009
Elsevier Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 1085-8725 1097-6825 |
| DOI | 10.1016/j.jaci.2009.05.030 |
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| Abstract | Rhinovirus infections are frequent causes of asthma exacerbations.
This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes.
Twenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation.
There were no group-specific significant differences in peak cold symptom scores (10.0 ± 5.8 vs 11.1 ± 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log
10 4.3 ± 0.8 vs 3.7 ± 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% ± 10% vs 8% ± 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 → 13;
P = .003) but only marginally in the healthy group (median, 4 → 7;
P = .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding.
These findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection. |
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| AbstractList | Rhinovirus infections are frequent causes of asthma exacerbations.
This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes.
Twenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation.
There were no group-specific significant differences in peak cold symptom scores (10.0 ± 5.8 vs 11.1 ± 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log
10 4.3 ± 0.8 vs 3.7 ± 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% ± 10% vs 8% ± 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 → 13;
P = .003) but only marginally in the healthy group (median, 4 → 7;
P = .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding.
These findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection. Rhinovirus infections are frequent causes of asthma exacerbations.BACKGROUNDRhinovirus infections are frequent causes of asthma exacerbations.This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes.OBJECTIVEThis study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes.Twenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation.METHODSTwenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation.There were no group-specific significant differences in peak cold symptom scores (10.0 +/- 5.8 vs 11.1 +/- 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log(10) 4.3 +/- 0.8 vs 3.7 +/- 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% +/- 10% vs 8% +/- 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 --> 13; P = .003) but only marginally in the healthy group (median, 4 --> 7; P = .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding.RESULTSThere were no group-specific significant differences in peak cold symptom scores (10.0 +/- 5.8 vs 11.1 +/- 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log(10) 4.3 +/- 0.8 vs 3.7 +/- 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% +/- 10% vs 8% +/- 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 --> 13; P = .003) but only marginally in the healthy group (median, 4 --> 7; P = .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding.These findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection.CONCLUSIONSThese findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection. Background Rhinovirus infections are frequent causes of asthma exacerbations. Objective This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes. Methods Twenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation. Results There were no group-specific significant differences in peak cold symptom scores (10.0 ± 5.8 vs 11.1 ± 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log104.3 ± 0.8 vs 3.7 ± 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% ± 10% vs 8% ± 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 [arrow right] 13;P= .003) but only marginally in the healthy group (median, 4 [arrow right] 7;P= .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding. Conclusions These findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection. Background Rhinovirus infections are frequent causes of asthma exacerbations. Objective This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes. Methods Twenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation. Results There were no group-specific significant differences in peak cold symptom scores (10.0 ± 5.8 vs 11.1 ± 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log10 4.3 ± 0.8 vs 3.7 ± 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% ± 10% vs 8% ± 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 → 13; P = .003) but only marginally in the healthy group (median, 4 → 7; P = .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding. Conclusions These findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection. Rhinovirus infections are frequent causes of asthma exacerbations. This study was conducted to test whether subjects with and without allergic asthma have different responses to infection and to identify baseline patient risk factors that predict cold outcomes. Twenty subjects with mild persistent allergic asthma and 18 healthy subjects were experimentally inoculated with rhinovirus-16. Subjects were evaluated at baseline, during the acute infection, and during recovery for asthma and cold symptoms by using a validated questionnaire. Sputum and nasal lavage fluid were evaluated for viral shedding, cytokines, and cellular inflammation. There were no group-specific significant differences in peak cold symptom scores (10.0 +/- 5.8 vs 11.1 +/- 6.2, asthmatic vs healthy subjects), peak nasal viral titers (log(10) 4.3 +/- 0.8 vs 3.7 +/- 1.4 50% tissue culture infective dose/mL, respectively), or changes in peak flow during the study (10% +/- 10% vs 8% +/- 6%, respectively). Rhinovirus-16 infection increased peak asthma index values in the asthmatic group (median, 6 --> 13; P = .003) but only marginally in the healthy group (median, 4 --> 7; P = .09). More asthmatic subjects had detectable eosinophils in nasal lavage and sputum samples at baseline and during infection, but otherwise, cellular and cytokine responses were similar. Baseline sputum eosinophilia and CXCL8 (IL-8) levels were positively associated with cold symptoms, whereas CCL2 (monocyte chemotactic protein 1) levels were inversely associated with nasal viral shedding. These findings suggest that subjects with mild allergic asthma and healthy subjects have similar cold symptoms and inflammatory and antiviral responses. In addition, eosinophilia and other selective baseline measures of airway inflammation in subjects with or without asthma might predict respiratory outcomes with rhinovirus infection. |
| Author | Sorkness, Ronald Weisshaar, Elizabeth H. Swenson, Cheri A. Evans, Michael D. Kakumanu, Sujani Morin, Allison DeMore, Jennifer P. Vrtis, Rose F. Gern, James E. Hazel, Elizabeth Bork, Jack A. Busse, William W. |
| Author_xml | – sequence: 1 givenname: Jennifer P. surname: DeMore fullname: DeMore, Jennifer P. email: jpd@medicine.wisc.edu organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 2 givenname: Elizabeth H. surname: Weisshaar fullname: Weisshaar, Elizabeth H. organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 3 givenname: Rose F. surname: Vrtis fullname: Vrtis, Rose F. organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 4 givenname: Cheri A. surname: Swenson fullname: Swenson, Cheri A. organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 5 givenname: Michael D. surname: Evans fullname: Evans, Michael D. organization: Department of Biostatistics and Medical Informatics, University of Wisconsin–Madison, Madison, Wis – sequence: 6 givenname: Allison surname: Morin fullname: Morin, Allison organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 7 givenname: Elizabeth surname: Hazel fullname: Hazel, Elizabeth organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 8 givenname: Jack A. surname: Bork fullname: Bork, Jack A. organization: Department of Pediatrics, University of Wisconsin–Madison, Madison, Wis – sequence: 9 givenname: Sujani surname: Kakumanu fullname: Kakumanu, Sujani organization: William S. Middleton VA Hospital, Madison, Wis – sequence: 10 givenname: Ronald surname: Sorkness fullname: Sorkness, Ronald organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 11 givenname: William W. surname: Busse fullname: Busse, William W. organization: Department of Medicine, University of Wisconsin–Madison, Madison, Wis – sequence: 12 givenname: James E. surname: Gern fullname: Gern, James E. organization: Department of Pediatrics, University of Wisconsin–Madison, Madison, Wis |
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| Snippet | Rhinovirus infections are frequent causes of asthma exacerbations.
This study was conducted to test whether subjects with and without allergic asthma have... Background Rhinovirus infections are frequent causes of asthma exacerbations. Objective This study was conducted to test whether subjects with and without... Rhinovirus infections are frequent causes of asthma exacerbations.BACKGROUNDRhinovirus infections are frequent causes of asthma exacerbations.This study was... |
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| SubjectTerms | Adult allergy Allergy and Immunology Asthma Asthma - immunology Asthma - virology Biological and medical sciences CCL2 Chronic obstructive pulmonary disease, asthma Colds common cold Common Cold - complications CXCL8 Cytokines - biosynthesis Cytokines - immunology Drug therapy eosinophil Eosinophils - immunology Eosinophils - metabolism Eosinophils - virology Female Fundamental and applied biological sciences. Psychology Fundamental immunology Humans Immunoglobulin E - blood Immunopathology Infections Male Medical sciences Nasal Lavage Fluid - virology Picornaviridae Infections - complications Pneumology Rhinovirus RNA, Viral - analysis Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis Sputum - metabolism Sputum - virology total serum IgE viral respiratory tract infections virus-induced asthma |
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| Title | Similar colds in subjects with allergic asthma and nonatopic subjects after inoculation with rhinovirus-16 |
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