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 (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. 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 (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. 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.
Authors: P C Avila; J A Abisheganaden; H Wong; J Liu; S Yagi; D Schnurr; J L Kishiyama; H A Boushey Journal: J Allergy Clin Immunol Date: 2000-05 Impact factor: 10.793
Authors: Jonathan M Corne; Clare Marshall; Sandra Smith; Jacquie Schreiber; Gwendolyn Sanderson; Stephen T Holgate; Sebastian L Johnston Journal: Lancet Date: 2002-03-09 Impact factor: 79.321
Authors: Shinichi Konno; Kristine A Grindle; Wai-Ming Lee; Mary K Schroth; Anne G Mosser; Rebecca A Brockman-Schneider; William W Busse; James E Gern Journal: Am J Respir Cell Mol Biol Date: 2002-05 Impact factor: 6.914
Authors: Lyndsey M Muehling; Peter W Heymann; Paul W Wright; Jacob D Eccles; Rachana Agrawal; Holliday T Carper; Deborah D Murphy; Lisa J Workman; Carolyn R Word; Sarah J Ratcliffe; Brian J Capaldo; Thomas A E Platts-Mills; Ronald B Turner; William W Kwok; Judith A Woodfolk Journal: J Allergy Clin Immunol Date: 2020-04-19 Impact factor: 10.793
Authors: Loren C Denlinger; Ron L Sorkness; Wai-Ming Lee; Michael D Evans; Michele J Wolff; Sameer K Mathur; Gina M Crisafi; Katie L Gaworski; Tressa E Pappas; Rose F Vrtis; Elizabeth A Kelly; James E Gern; Nizar N Jarjour Journal: Am J Respir Crit Care Med Date: 2011-11-01 Impact factor: 21.405
Authors: Kazuyuki Nakagome; Yury A Bochkov; Shamaila Ashraf; Rebecca A Brockman-Schneider; Michael D Evans; Thomas R Pasic; James E Gern Journal: J Allergy Clin Immunol Date: 2014-03-14 Impact factor: 10.793
Authors: Sameer K Mathur; Paul S Fichtinger; John T Kelly; Wai-Ming Lee; James E Gern; Nizar N Jarjour Journal: Ann Allergy Asthma Immunol Date: 2013-07 Impact factor: 6.347
Authors: Peter W Heymann; Thomas A E Platts-Mills; Judith A Woodfolk; Larry Borish; Deborah D Murphy; Holliday T Carper; Mark R Conaway; John W Steinke; Lyndsey Muehling; W Gerald Teague; Joshua L Kennedy; Anne-Marie Irani; Matthew D McGraw; Stephen V Early; Lisa M Wheatley; Amy P Adams; Ronald B Turner Journal: J Allergy Clin Immunol Date: 2020-02-01 Impact factor: 10.793