Experimental rhinovirus challenges in adults with mild asthma: Response to infection in relation to IgE
Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV). Young atopic adults with mild asthma were evaluated before and during an experimental HRV infection...
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Published in | Journal of allergy and clinical immunology Vol. 111; no. 5; pp. 1008 - 1016 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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New York, NY
Mosby, Inc
01.05.2003
Elsevier Elsevier Limited |
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Abstract | Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV).
Young atopic adults with mild asthma were evaluated before and during an experimental HRV infection to test the hypothesis that airway inflammation before virus inoculation may be a risk factor for an adverse response to HRV.
Experimental HRV infections were evaluated in 16 allergic volunteers with mild asthma and 9 nonatopic control patients (age, 18 to 30 years). Before virus inoculation, each participant was screened with tests for lung function, prick skin tests for sensitization to common aeroallergens, measurements of total serum IgE, and serum neutralizing antibody to rhinovirus-16 (the serotype used for inoculation). The response to infection was monitored for 21 days by using symptom diary cards, tests for lung function, and markers of airway inflammation in nasal washes, blood, and expired air.
During the infection, asthmatic patients had cumulative upper and lower respiratory tract symptom scores that were significantly greater over the course of 21 days than scores from the control patients. At baseline, the asthmatic patients also had increased sensitivity to methacholine and significantly lower values for FEV1 (percent predicted) than the control patients (geometric mean and intraquartile values: 87% [79% to 91%] for the asthmatic patients and 101% [90% to 104%] for the control patients, P<.03). Among the patients with mild asthma, 6 had levels of total serum IgE that were substantially elevated (range, 371 to 820 IU/mL). Those with high levels of IgE had significantly greater lower respiratory tract symptom scores during the initial 4 days of the infection than the low IgE group. They also had higher total blood eosinophil counts at baseline, increased eosinophil cationic protein in their nasal washes (>200 ng/mL), and augmented levels of expired nitric oxide at baseline and during peak cold symptoms. In contrast, levels of soluble intracellular adhesion molecule-1 in nasal wash supernatants from the asthmatic patients with high IgE were diminished, both at baseline and during the infection.
The reduced lung function and increased markers of inflammation observed before virus inoculation in the asthmatic patients who had high levels of total serum IgE may be risk factors for an adverse response to infections with HRV. |
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AbstractList | Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV).
Young atopic adults with mild asthma were evaluated before and during an experimental HRV infection to test the hypothesis that airway inflammation before virus inoculation may be a risk factor for an adverse response to HRV.
Experimental HRV infections were evaluated in 16 allergic volunteers with mild asthma and 9 nonatopic control patients (age, 18 to 30 years). Before virus inoculation, each participant was screened with tests for lung function, prick skin tests for sensitization to common aeroallergens, measurements of total serum IgE, and serum neutralizing antibody to rhinovirus-16 (the serotype used for inoculation). The response to infection was monitored for 21 days by using symptom diary cards, tests for lung function, and markers of airway inflammation in nasal washes, blood, and expired air.
During the infection, asthmatic patients had cumulative upper and lower respiratory tract symptom scores that were significantly greater over the course of 21 days than scores from the control patients. At baseline, the asthmatic patients also had increased sensitivity to methacholine and significantly lower values for FEV1 (percent predicted) than the control patients (geometric mean and intraquartile values: 87% [79% to 91%] for the asthmatic patients and 101% [90% to 104%] for the control patients, P<.03). Among the patients with mild asthma, 6 had levels of total serum IgE that were substantially elevated (range, 371 to 820 IU/mL). Those with high levels of IgE had significantly greater lower respiratory tract symptom scores during the initial 4 days of the infection than the low IgE group. They also had higher total blood eosinophil counts at baseline, increased eosinophil cationic protein in their nasal washes (>200 ng/mL), and augmented levels of expired nitric oxide at baseline and during peak cold symptoms. In contrast, levels of soluble intracellular adhesion molecule-1 in nasal wash supernatants from the asthmatic patients with high IgE were diminished, both at baseline and during the infection.
The reduced lung function and increased markers of inflammation observed before virus inoculation in the asthmatic patients who had high levels of total serum IgE may be risk factors for an adverse response to infections with HRV. Background: Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV). Objective: Young atopic adults with mild asthma were evaluated before and during an experimental HRV infection to test the hypothesis that airway inflammation before virus inoculation may be a risk factor for an adverse response to HRV. Methods: Experimental HRV infections were evaluated in 16 allergic volunteers with mild asthma and 9 nonatopic control patients (age, 18 to 30 years). Before virus inoculation, each participant was screened with tests for lung function, prick skin tests for sensitization to common aeroallergens, measurements of total serum IgE, and serum neutralizing antibody to rhinovirus-16 (the serotype used for inoculation). The response to infection was monitored for 21 days by using symptom diary cards, tests for lung function, and markers of airway inflammation in nasal washes, blood, and expired air. Results: During the infection, asthmatic patients had cumulative upper and lower respiratory tract symptom scores that were significantly greater over the course of 21 days than scores from the control patients. At baseline, the asthmatic patients also had increased sensitivity to methacholine and significantly lower values for FEV1(percent predicted) than the control patients (geometric mean and intraquartile values: 87% [79% to 91%] for the asthmatic patients and 101% [90% to 104%] for the control patients,P<.03). Among the patients with mild asthma, 6 had levels of total serum IgE that were substantially elevated (range, 371 to 820 IU/mL). Those with high levels of IgE had significantly greater lower respiratory tract symptom scores during the initial 4 days of the infection than the low IgE group. They also had higher total blood eosinophil counts at baseline, increased eosinophil cationic protein in their nasal washes (>200 ng/mL), and augmented levels of expired nitric oxide at baseline and during peak cold symptoms. In contrast, levels of soluble intracellular adhesion molecule-1 in nasal wash supernatants from the asthmatic patients with high IgE were diminished, both at baseline and during the infection. Conclusions: The reduced lung function and increased markers of inflammation observed before virus inoculation in the asthmatic patients who had high levels of total serum IgE may be risk factors for an adverse response to infections with HRV. Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV). Young atopic adults with mild asthma were evaluated before and during an experimental HRV infection to test the hypothesis that airway inflammation before virus inoculation may be a risk factor for an adverse response to HRV. Experimental HRV infections were evaluated in 16 allergic volunteers with mild asthma and 9 nonatopic control patients (age, 18 to 30 years). Before virus inoculation, each participant was screened with tests for lung function, prick skin tests for sensitization to common aeroallergens, measurements of total serum IgE, and serum neutralizing antibody to rhinovirus-16 (the serotype used for inoculation). The response to infection was monitored for 21 days by using symptom diary cards, tests for lung function, and markers of airway inflammation in nasal washes, blood, and expired air. During the infection, asthmatic patients had cumulative upper and lower respiratory tract symptom scores that were significantly greater over the course of 21 days than scores from the control patients. At baseline, the asthmatic patients also had increased sensitivity to methacholine and significantly lower values for FEV(1) (percent predicted) than the control patients (geometric mean and intraquartile values: 87% [79% to 91%] for the asthmatic patients and 101% [90% to 104%] for the control patients, P <.03). Among the patients with mild asthma, 6 had levels of total serum IgE that were substantially elevated (range, 371 to 820 IU/mL) compared with 10 who had lower levels (range, 29 to 124 IU/mL). Those with high levels of IgE had significantly greater lower respiratory tract symptom scores during the initial 4 days of the infection than the low IgE group. They also had higher total blood eosinophil counts at baseline, increased eosinophil cationic protein in their nasal washes (>200 ng/mL), and augmented levels of expired nitric oxide at baseline and during peak cold symptoms. In contrast, levels of soluble intracellular adhesion molecule-1 in nasal wash supernatants from the asthmatic patients with high IgE were diminished, both at baseline and during the infection. The reduced lung function and increased markers of inflammation observed before virus inoculation in the asthmatic patients who had high levels of total serum IgE may be risk factors for an adverse response to infections with HRV. BACKGROUNDAlthough most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV).OBJECTIVEYoung atopic adults with mild asthma were evaluated before and during an experimental HRV infection to test the hypothesis that airway inflammation before virus inoculation may be a risk factor for an adverse response to HRV.METHODSExperimental HRV infections were evaluated in 16 allergic volunteers with mild asthma and 9 nonatopic control patients (age, 18 to 30 years). Before virus inoculation, each participant was screened with tests for lung function, prick skin tests for sensitization to common aeroallergens, measurements of total serum IgE, and serum neutralizing antibody to rhinovirus-16 (the serotype used for inoculation). The response to infection was monitored for 21 days by using symptom diary cards, tests for lung function, and markers of airway inflammation in nasal washes, blood, and expired air.RESULTSDuring the infection, asthmatic patients had cumulative upper and lower respiratory tract symptom scores that were significantly greater over the course of 21 days than scores from the control patients. At baseline, the asthmatic patients also had increased sensitivity to methacholine and significantly lower values for FEV(1) (percent predicted) than the control patients (geometric mean and intraquartile values: 87% [79% to 91%] for the asthmatic patients and 101% [90% to 104%] for the control patients, P <.03). Among the patients with mild asthma, 6 had levels of total serum IgE that were substantially elevated (range, 371 to 820 IU/mL) compared with 10 who had lower levels (range, 29 to 124 IU/mL). Those with high levels of IgE had significantly greater lower respiratory tract symptom scores during the initial 4 days of the infection than the low IgE group. They also had higher total blood eosinophil counts at baseline, increased eosinophil cationic protein in their nasal washes (>200 ng/mL), and augmented levels of expired nitric oxide at baseline and during peak cold symptoms. In contrast, levels of soluble intracellular adhesion molecule-1 in nasal wash supernatants from the asthmatic patients with high IgE were diminished, both at baseline and during the infection.CONCLUSIONSThe reduced lung function and increased markers of inflammation observed before virus inoculation in the asthmatic patients who had high levels of total serum IgE may be risk factors for an adverse response to infections with HRV. Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections, especially those caused by rhinovirus (HRV). Objective: Young atopic adults with mild asthma were evaluated before and during an experimental HRV infection to test the hypothesis that airway inflammation before virus inoculation may be a risk factor for an adverse response to HRV. Methods: Experimental HRV infections were evaluated in 16 allergic volunteers with mild asthma and 9 nonatopic control patients (age, 18 to 30 years). Before virus inoculation, each participant was screened with tests for lung function, prick skin tests for sensitization to common aeroallergens, measurements of total serum IgE, and serum neutralizing antibody to rhinovirus-16 (the serotype used for inoculation). The response to infection was monitored for 21 days by using symptom diary cards, tests for lung function, and markers of airway inflammation in nasal washes, blood, and expired air. Results: During the infection, asthmatic patients had cumulative upper and lower respiratory tract symptom scores that were significantly greater over the course of 21 days than scores from the control patients. At baseline, the asthmatic patients also had increased sensitivity to methacholine and significantly lower values for FEV sub(1) (percent predicted) than the control patients (geometric mean and intraquartile values: 87% [79% to 91%] for the asthmatic patients and 101% [90% to 104%] for the control patients, P < .03). Among the patients with mild asthma, 6 had levels of total serum IgE that were substantially elevated (range, 371 to 820 IU/mL) compared with 10 who had lower levels (range, 29 to 124 IU/mL). Those with high levels of IgE had significantly greater lower respiratory tract symptom scores during the initial 4 days of the infection than the low IgE group. They also had higher total blood eosinophil counts at baseline, increased eosinophil cationic protein in their nasal washes (>200 ng/mL), and augmented levels of expired nitric oxide at baseline and during peak cold symptoms. In contrast, levels of soluble intracellular adhesion molecule-1 in nasal wash supernatants from the asthmatic patients with high IgE were diminished, both at baseline and during the infection. Conclusions: The reduced lung function and increased markers of inflammation observed before virus inoculation in the asthmatic patients who had high levels of total serum IgE may be risk factors for an adverse response to infections with HRV. |
Author | Rakes, Gary P. Gwaltney, Jack M. Platts-Mills, Thomas A.E. Heymann, Peter W. Patrie, James Hayden, Frederick G. Hatley, Tina K. Zambrano, Juan C. Carper, Holliday T. Murphy, Deborah D. Owens, Angela M. |
Author_xml | – sequence: 1 givenname: Juan C. surname: Zambrano fullname: Zambrano, Juan C. organization: Department of Pediatrics University of Virginia Health System USA – sequence: 2 givenname: Holliday T. surname: Carper fullname: Carper, Holliday T. organization: Department of Pediatrics University of Virginia Health System USA – sequence: 3 givenname: Gary P. surname: Rakes fullname: Rakes, Gary P. organization: Department of Pediatrics University of Virginia Health System USA – sequence: 4 givenname: James surname: Patrie fullname: Patrie, James organization: Department of Health Evaluation Sciences University of Virginia Health System USA – sequence: 5 givenname: Deborah D. surname: Murphy fullname: Murphy, Deborah D. organization: Department of Pediatrics University of Virginia Health System USA – sequence: 6 givenname: Thomas A.E. surname: Platts-Mills fullname: Platts-Mills, Thomas A.E. organization: Department of Internal Medicine, University of Virginia Health System USA – sequence: 7 givenname: Frederick G. surname: Hayden fullname: Hayden, Frederick G. organization: Department of Internal Medicine, University of Virginia Health System USA – sequence: 8 givenname: Jack M. surname: Gwaltney fullname: Gwaltney, Jack M. organization: Department of Internal Medicine, University of Virginia Health System USA – sequence: 9 givenname: Tina K. surname: Hatley fullname: Hatley, Tina K. organization: Department of Pediatrics University of Virginia Health System USA – sequence: 10 givenname: Angela M. surname: Owens fullname: Owens, Angela M. organization: Department of Pediatrics University of Virginia Health System USA – sequence: 11 givenname: Peter W. surname: Heymann fullname: Heymann, Peter W. organization: Department of Pediatrics University of Virginia Health System USA |
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Keywords | viral infections allergic inflammation eosinophil cationic protein IgE intracellular adhesion molecule-1 eosinophils expired nitric oxide rhinovirus Asthma Immunopathology Allergy Intercellular adhesion molecule 1 Respiratory disease Picornaviridae Granulocyte Inflammation Eosinophil Virus Infection Nitric oxide Obstructive pulmonary disease Eosinophil cationic protein Rhinovirus |
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PublicationPlace_xml | – name: New York, NY – name: United States – name: St. Louis |
PublicationTitle | Journal of allergy and clinical immunology |
PublicationTitleAlternate | J Allergy Clin Immunol |
PublicationYear | 2003 |
Publisher | Mosby, Inc Elsevier Elsevier Limited |
Publisher_xml | – name: Mosby, Inc – name: Elsevier – name: Elsevier Limited |
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protect against the effects of a rhinovirus cold? publication-title: J Allergy Clin Immunol doi: 10.1067/mai.2000.106378 contributor: fullname: Busse – volume: 320 start-page: 271 year: 1989 ident: 10.1067/mai.2003.1396_bib6 article-title: Association of asthma with serum IgE levels and skin-test reactivity to allergens publication-title: N Engl J Med doi: 10.1056/NEJM198902023200502 contributor: fullname: Burrows |
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Snippet | Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract infections,... Background: Although most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract... BACKGROUNDAlthough most children and young adults with asthma are atopic, exacerbations of asthma are frequently associated with viral respiratory tract... |
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SubjectTerms | Adolescent Adult allergic inflammation Asthma Asthma - immunology Biological and medical sciences Blood Proteins - analysis Chronic obstructive pulmonary disease, asthma Common Cold eosinophil cationic protein Eosinophil Granule Proteins eosinophils expired nitric oxide Female Human viral diseases Humans IgE Immunoglobulin E - blood Infectious diseases Intercellular Adhesion Molecule-1 - analysis intracellular adhesion molecule-1 Lung - physiopathology Male Medical sciences Nasal Mucosa - chemistry Nitric Oxide - biosynthesis Picornaviridae Infections - etiology Picornaviridae Infections - immunology Pneumology Rhinovirus Ribonucleases Viral diseases Viral diseases of the respiratory system and ent viral diseases viral infections |
Title | Experimental rhinovirus challenges in adults with mild asthma: Response to infection in relation to IgE |
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