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Effect of experimental rhinovirus 16 colds on airway hyperresponsiveness to histamine and interleukin-8 in nasal lavage in asthmatic subjects in vivo.

Abstract

BACKGROUND

Asthma exacerbations are closely associated with respiratory virus infections. However, the pathophysiological consequences of such infections in asthma are largely unclear.

OBJECTIVE

To examine the effect of rhinovirus 16 (RV16) infection on airway hypersensitivity to histamine, and on interleukin-8 (IL-8) in nasal lavage.

METHODS

Twenty-seven non-smoking atopic, mildly asthmatic subjects participated in a placebo-controlled, parallel study. A dose of 0.5-2.9 x 10(4) TCID50 RV16 or placebo was nasally administered. Cold symptoms were recorded by questionnaire throughout the study. Histamine challenges were performed at entry, and on days 4 and 11 after inoculation. Nasal lavages were obtained at entry, and on days 2 and 9. The response to histamine was measured by PC20 (changes expressed as doubling doses: DD) IL-8 levels were obtained by ELISA, and were expressed in ng/ml.

RESULTS

RV infection was confirmed by culture of nasal lavage and/or by antibody titre rise in each of the RV16-treated subjects. Among the 19 RV 16-treated subjects, eight developed severe cold symptoms. Baseline FEV1, did not change significantly during the study in either treatment group (P = 0.99). However, in the RV16-treated subjects there was a decrease in PC20 at day 4, which was most pronounced in those with a severe cold (mean change +/- SEM: -1.14 +/- 0.28 DD, P = 0.01). In addition, IL-8 levels increased in the RV16 group at days 2 and 9 (P < 0.001). The increase in nasal IL-8 at day 2 correlated significantly with the change in PC20 at day 4 (r = -0.48, P = 0.04).

CONCLUSION

We conclude that the severity of cold, as induced by experimental RV16 infection, is a determinant of the increase in airway hypersensitivity to histamine in patients with asthma. Our results suggest that this may be mediated by an inflammatory mechanism, involving the release of chemokines such as IL-8.

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  • Authors+Show Affiliations

    ,

    Department of Pulmonology, Leiden University Medical Centre, The Netherlands.

    , , , , , ,

    Source

    MeSH

    Adolescent
    Adult
    Asthma
    Bronchial Hyperreactivity
    Bronchial Provocation Tests
    Common Cold
    Double-Blind Method
    Enzyme-Linked Immunosorbent Assay
    Female
    Forced Expiratory Volume
    Histamine
    Humans
    Interleukin-8
    Leukocyte Count
    Lung
    Male
    Nasal Lavage Fluid
    Rhinovirus

    Pub Type(s)

    Clinical Trial
    Journal Article
    Randomized Controlled Trial
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    9117878

    Citation

    Grünberg, K, et al. "Effect of Experimental Rhinovirus 16 Colds On Airway Hyperresponsiveness to Histamine and Interleukin-8 in Nasal Lavage in Asthmatic Subjects in Vivo." Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, vol. 27, no. 1, 1997, pp. 36-45.
    Grünberg K, Timmers MC, Smits HH, et al. Effect of experimental rhinovirus 16 colds on airway hyperresponsiveness to histamine and interleukin-8 in nasal lavage in asthmatic subjects in vivo. Clin Exp Allergy. 1997;27(1):36-45.
    Grünberg, K., Timmers, M. C., Smits, H. H., de Klerk, E. P., Dick, E. C., Spaan, W. J., ... Sterk, P. J. (1997). Effect of experimental rhinovirus 16 colds on airway hyperresponsiveness to histamine and interleukin-8 in nasal lavage in asthmatic subjects in vivo. Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology, 27(1), pp. 36-45.
    Grünberg K, et al. Effect of Experimental Rhinovirus 16 Colds On Airway Hyperresponsiveness to Histamine and Interleukin-8 in Nasal Lavage in Asthmatic Subjects in Vivo. Clin Exp Allergy. 1997;27(1):36-45. PubMed PMID: 9117878.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Effect of experimental rhinovirus 16 colds on airway hyperresponsiveness to histamine and interleukin-8 in nasal lavage in asthmatic subjects in vivo. AU - Grünberg,K, AU - Timmers,M C, AU - Smits,H H, AU - de Klerk,E P, AU - Dick,E C, AU - Spaan,W J, AU - Hiemstra,P S, AU - Sterk,P J, PY - 1997/1/1/pubmed PY - 1997/1/1/medline PY - 1997/1/1/entrez SP - 36 EP - 45 JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology JO - Clin. Exp. Allergy VL - 27 IS - 1 N2 - BACKGROUND: Asthma exacerbations are closely associated with respiratory virus infections. However, the pathophysiological consequences of such infections in asthma are largely unclear. OBJECTIVE: To examine the effect of rhinovirus 16 (RV16) infection on airway hypersensitivity to histamine, and on interleukin-8 (IL-8) in nasal lavage. METHODS: Twenty-seven non-smoking atopic, mildly asthmatic subjects participated in a placebo-controlled, parallel study. A dose of 0.5-2.9 x 10(4) TCID50 RV16 or placebo was nasally administered. Cold symptoms were recorded by questionnaire throughout the study. Histamine challenges were performed at entry, and on days 4 and 11 after inoculation. Nasal lavages were obtained at entry, and on days 2 and 9. The response to histamine was measured by PC20 (changes expressed as doubling doses: DD) IL-8 levels were obtained by ELISA, and were expressed in ng/ml. RESULTS: RV infection was confirmed by culture of nasal lavage and/or by antibody titre rise in each of the RV16-treated subjects. Among the 19 RV 16-treated subjects, eight developed severe cold symptoms. Baseline FEV1, did not change significantly during the study in either treatment group (P = 0.99). However, in the RV16-treated subjects there was a decrease in PC20 at day 4, which was most pronounced in those with a severe cold (mean change +/- SEM: -1.14 +/- 0.28 DD, P = 0.01). In addition, IL-8 levels increased in the RV16 group at days 2 and 9 (P < 0.001). The increase in nasal IL-8 at day 2 correlated significantly with the change in PC20 at day 4 (r = -0.48, P = 0.04). CONCLUSION: We conclude that the severity of cold, as induced by experimental RV16 infection, is a determinant of the increase in airway hypersensitivity to histamine in patients with asthma. Our results suggest that this may be mediated by an inflammatory mechanism, involving the release of chemokines such as IL-8. SN - 0954-7894 UR - https://www.unboundmedicine.com/medline/citation/9117878/Effect_of_experimental_rhinovirus_16_colds_on_airway_hyperresponsiveness_to_histamine_and_interleukin_8_in_nasal_lavage_in_asthmatic_subjects_in_vivo_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&amp;sid=nlm:pubmed&amp;issn=0954-7894&amp;date=1997&amp;volume=27&amp;issue=1&amp;spage=36 DB - PRIME DP - Unbound Medicine ER -