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Respiratory viral infections as promoters of allergic sensitization and asthma in animal models

¹ Children's Hospital, St Josef-Hospital Bochum, Ruhr-University Bochum, Bochum, Germany and ² Division of Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO, USA

CORRESPONDENCE: J. Schwarze, Klinik für Kinder- und Jugendmedizin im St Josef-Hospital Bochum, Alexandrinenstr. 5, 44791, Bochum, Germany. Fax: 49 234 5092612. E-mail: juergen.schwarze@ruhr-uni-bochum.de

Keywords: airway inflammation, airway obstruction, allergic sensitization, animal models, asthma, respiratory virus infection

Received: January 15, 2001
Accepted June 20, 2001

This study was supported by Grants HL-61005 and HL-36577 (E.W. Gelfand) from the National Institutes of Health, Grant Schw 597/1-1 from the Deutsche Forschungsgemeinschaft and Grant 01GC9802 (J. Schwarze) from the Bundesministerium für Bildung und Forschung.

Abstract

Respiratory virus infections can trigger exacerbations of asthma and may also contribute to allergic sensitization to aeroallergens and the development of asthma. Conversely, atopy may predispose to more severe virus-induced airway disease. The animal models reviewed in this article support the hypothesis that respiratory virus infections can promote allergic sensitization and the development of asthma. Respiratory viruses can prevent induction of tolerance and enhance sensitization to inhaled allergens resulting in increased airway inflammation and airway hyperresponsiveness.

Probable mechanisms involved in this enhanced sensitization are increased permeability of the airway mucosa to allergens and recruitment of dendritic cells to the respiratory epithelium during acute infection. Factors involved in augmenting the consequences of allergic airway sensitization appear to be T-cells, especially CD8+ T-cells as regulators of this process, interleukin-5 as a pivotal cytokine for eosinophilic airway inflammation and eosinophils themselves as effector cells triggering airway hyperresponsiveness. Depending on the timing of allergen exposure, respiratory virus infections which elicit a significant type 1 T-helper cell cytokine response may also downregulate allergic sensitization.

Respiratory virus infections in animals previously sensitized to aeroallergens result in prolonged increases in inflammation and airway responsiveness, indicating that critical interactions between immune responses to allergen sensitization and the responses to infection can lead to more severe disease.

Taken together, animal models have proved valuable in generating a number of plausible pathogenetic concepts, and can be used to address a host of unresolved questions regarding the immunology of respiratory virus infections, allergic sensitization and asthma.

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