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June 2000

Volume 181, Number 6
The Journal of Infectious Diseases 2000;181:1875–1884
© 2000 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2000/18106-0001$02.00
DOI: 10.1086/315513

Rhinoviruses Infect the Lower Airways

Nikolaos G. Papadopoulos,a

Philip J. Bates,

Philip G. Bardin,a

Alberto Papi,

Shih H. Leir,

David J. Fraenkel,

Jon Meyer,

Peter M. Lackie,

Gwendolyn Sanderson,

Stephen T. Holgate, and

Sebastian L. Johnstona

University Medicine, Southampton General Hospital, Southampton, United Kingdom

Abstract

Rhinoviruses are the major cause of the common cold and a trigger of acute asthma exacerbations. Whether these exacerbations result from direct infection of the lower airway or from indirect mechanisms consequent on infection of the upper airway alone is currently unknown. Lower respiratory infection was investigated in vitro by exposing primary human bronchial epithelial cells to rhinoviruses and in vivo after experimental upper respiratory infection of human volunteers. Bronchial infection was confirmed by both approaches. Furthermore, rhinoviruses induced production of interleukin‐6, ‐8, and ‐16 and RANTES and were cytotoxic to cultured respiratory epithelium. This evidence strongly supports a direct lower respiratory epithelial reaction as the initial event in the induction of rhinovirus‐mediated asthma exacerbations. The frequency of infection and the nature of the inflammatory response observed are similar to those of the upper respiratory tract, suggesting that rhinovirus infections may be one of the most important causes of lower in addition to upper respiratory disease.

Received 17 November 1999; revised 8 February 2000; electronically published 5 June 2000.

Reprints or correspondence: Dr. S. L. Johnston, National Heart and Lung Institute, Dept. of Respiratory Medicine, Imperial College School of Medicine at St. Mary’s, Norfolk Pl., London W2 1PG, United Kingdom ().

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  • Presented in part: annual meeting of the American Thoracic Society, San Diego, 23–28 April, 1999 (abstract B29).

    Informed consent was obtained from the subjects of this study, which was approved by the Southampton University and Hospitals Joint Ethics Subcommittee.

    Grant support: Medical Research Council (grants G9328737 to P.G.B., S.T.H., and S.L.J. and G8604034 to S.T.H.), the National Asthma Campaign (grant 332 to S.L.J.), the Wessex Medical Trust (to P.J.B. and S.L.J.), the Royal Society (to P.J.B. and S.L.J.), and the University of Ferrara (to A.P.).

  • aPresent affiliations: Allergy and Clinical Immunology Unit, Second Pediatric Clinic, University of Athens, Athens, Greece (N.G.P.); Lung Unit, Internal Medicine, University of Stellenbosch, Tygerberg, Cape Town, South Africa (P.G.B); National Heart and Lung Institute, Department of Respiratory Medicine, Imperial College School of Medicine at St. Mary's, London, United Kingdom (S.L.J.).

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