The Journal of Allergy and Clinical Immunology
Volume 124, Issue 2 , Pages 245-252.e3, August 2009

Similar colds in subjects with allergic asthma and nonatopic subjects after inoculation with rhinovirus-16

  • Jennifer P. DeMore, MD

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
    • Corresponding Author InformationReprint requests: Jennifer P. DeMore, MD, K4/910 CSC 9988, 600 Highland Ave, Madison, WI 53792.
  • ,
  • Elizabeth H. Weisshaar, BS

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
  • ,
  • Rose F. Vrtis, BS

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
  • ,
  • Cheri A. Swenson, BS

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
  • ,
  • Michael D. Evans, MS

      Affiliations

    • Department of Biostatistics and Medical Informatics, University of Wisconsin–Madison, Madison, Wis
  • ,
  • Allison Morin, BS

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
  • ,
  • Elizabeth Hazel, MHS

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
  • ,
  • Jack A. Bork, BS

      Affiliations

    • Department of Pediatrics, University of Wisconsin–Madison, Madison, Wis
  • ,
  • Sujani Kakumanu, MD

      Affiliations

    • William S. Middleton VA Hospital, Madison, Wis
  • ,
  • Ronald Sorkness, PhD

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
    • Department of Pediatrics, University of Wisconsin–Madison, Madison, Wis
    • School of Pharmacy, University of Wisconsin–Madison, Madison, Wis
  • ,
  • William W. Busse, MD

      Affiliations

    • Department of Medicine, University of Wisconsin–Madison, Madison, Wis
  • ,
  • James E. Gern, MD

      Affiliations

    • Department of Pediatrics, University of Wisconsin–Madison, Madison, Wis

Received 16 September 2008; received in revised form 26 May 2009; accepted 26 May 2009. published online 14 July 2009.

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.

Key words: Asthma, viral respiratory tract infections, virus-induced asthma, rhinovirus, eosinophil, CCL2, CXCL8, total serum IgE, allergy, common cold

Abbreviations used: PEF, Peak expiratory flow, PFU, Plaque-forming units, RV16, Rhinovirus-16, TCID50, 50% Tissue culture infective dose, TDHSS, Total daily highest symptom score

 

 Supported by funds from National Institutes of Health and National Institute of Allergy and Infectious Diseases grants P01 AI50500 and U19 AI070503-01.

 Disclosure of potential conflict of interest: R. Sorkness receives research support from the National Institutes of Health and Modus Biological Membranes. W. W. Busse is on the advisory board/a consultant for Genentech/Novartis, Altair, GlaxoSmithKline, Altana, Wyeth, Pfizer, Dynavax, Centocor, and Schering-Plough; is a speaker for GlaxoSmithKline, Novartis, Merck, and AstraZeneca; and received research support from Novartis, Dynavax, Wyeth, Centocor, and GlaxoSmithKline. The rest of the authors have declared that they have no conflict of interest.

PII: S0091-6749(09)00854-9

doi:10.1016/j.jaci.2009.05.030

The Journal of Allergy and Clinical Immunology
Volume 124, Issue 2 , Pages 245-252.e3, August 2009