Allergic airway inflammation is exacerbated during acute influenza infection and correlates with increased allergen presentation and recruitment of allergen-specific T-helper type 2 cells

• Published in: Clinical and experimental allergy 2004-08, Vol.34 (8), p.1299-1306
• Main Authors: Marsland, B. J., Scanga, C. B., Kopf, M., Le Gros, G.
• Format: Article
• Language: English
• Subjects: Acute Disease; Allergens - immunology; Allergic diseases; Animals; asthma; Asthma - immunology; Asthma - virology; Biological and medical sciences; Bronchi - immunology; exacerbation; Flow Cytometry; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Immunologic Memory; Immunopathology; influenza; Medical sciences; Mice; Mice, Inbred C57BL; Mice, Transgenic; Models, Animal; Orthomyxoviridae Infections - immunology; Ovalbumin; Plethysmography; Receptors, Antigen, T-Cell - genetics; T cell; Th2 Cells - immunology; virus
• ISSN: 0954-7894; 1365-2222
• DOI: 10.1111/j.1365-2222.2004.02021.x

Summary Background Respiratory viral infections are a leading cause of the hospitalization of asthmatics, however, the cellular immunological interactions which underlie these two diseases remain elusive. Objective We sought to characterize the effect influenza viral infection has on allergic airway inflammation and to identify the cellular pathways involved. Methods We have used an ovalbumin (OVA) model of allergic airway inflammation, which involves sensitization of animals with OVA adsorbed in alum adjuvant followed by an intranasal challenge with OVA in phosphate‐buffered saline. To study T cell recruitment into the lung, we adoptively transferred in vitro activated T cell receptor‐transgenic T cells, which were subsequently identified by fluorescence‐activated cell sorting (FACS) analysis. In addition, to study in vivo dendritic cell (DC) migration, we administered fluorescently labelled dextran and identified DCs that had phagocytosed it by FACS analysis. Results We found that different stages of influenza infection had contrasting effects upon the outcome of OVA‐induced allergic airway inflammation. The allergic response against OVA was exacerbated during the acute stage of influenza infection; however, mice were protected against the development of airway eosinophilia at late time‐points following infection. We investigated the mechanisms responsible for the virus‐induced exacerbation and found that the response was partially independent of IL‐4 and that there was increased delivery of inhaled allergens to the draining lymph node during the acute stage of the infection. In addition, virus‐induced inflammation in the lung and draining lymph node resulted in the non‐specific recruitment of circulating allergen‐specific effector/memory cells. Conclusion In addition to virus‐mediated damage to the lung and airways, influenza viral infection can also enhance unrelated local allergic responses.