Respiratory syncytial virus infection does not increase allergen-induced type 2 cytokine production, yet increases airway hyperresponsiveness in mice

Severe respiratory syncytial virus (RSV)‐induced disease is associated with childhood asthma and atopy. We combined murine models of allergen‐sensitization and RSV infection to explore the interaction of allergic and virus‐induced airway inflammation and its impact on airway hyperresponsiveness (AHR...

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Published in:	Journal of medical virology Vol. 63; no. 2; pp. 178 - 188
Main Authors:	Peebles Jr, R. Stokes, Sheller, James R., Collins, Robert D., Jarzecka, A. Kasia, Mitchell, Daphne B., Parker, Robert A., Graham, Barney S.
Format:	Journal Article
Language:	English
Published:	New York John Wiley & Sons, Inc 01-02-2001 Wiley-Liss
Subjects:	airway hyperresponsiveness Allergens - immunology Animals Biological and medical sciences bronchoalveolar lavage Cytokines - analysis Cytokines - metabolism Disease Models, Animal Experimental viral diseases and models Female Flow Cytometry Hypersensitivity - immunology Immunization immunoglobulin E Infectious diseases interferon interleukin Interleukin-13 - metabolism Interleukin-4 - metabolism Interleukin-5 - metabolism Lung - immunology Lymphocytes - immunology Medical sciences Mice Mice, Inbred BALB C Ovalbumin - immunology periodic acid-Schiff respiratory syncytial virus Respiratory Syncytial Virus Infections - immunology Respiratory Syncytial Viruses RNA, Messenger - analysis Specific Pathogen-Free Organisms Viral diseases Human respiratory syncytial virus Allergy Animal model Upper respiratory tract Pathogenesis IgE Paramyxoviridae Atopy Sensitization Obstructive pulmonary disease Pneumovirus Immunopathology Pneumovirinae Respiratory disease Rodentia Cytokine Inflammation Asthma Infection Virus Mononegavirales Vertebrata Mammalia Mouse Viral disease
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Summary:	Severe respiratory syncytial virus (RSV)‐induced disease is associated with childhood asthma and atopy. We combined murine models of allergen‐sensitization and RSV infection to explore the interaction of allergic and virus‐induced airway inflammation and its impact on airway hyperresponsiveness (AHR). We found that RSV infection during ova‐sensitization (OVA/RSV) increasedtlsb and prolonged AHR compared to mice only RSV‐infected (RSV) or ova‐sensitized (OVA). AHR is known to be associated with an increase in Type 2 cytokines (IL‐4, IL‐5, and IL‐13) in allergen‐sensitized mice. Therefore, we hypothesized that RSV‐induced enhancement of AHR was a result of potentiating the Type 2 cytokine profile promoted by ova‐sensitization. Surprisingly, we found that Type 2 cytokines induced by ova‐sensitization were not increased by RSV infection despite the increase in AHR, and in some cases were diminished. RNAse protection assay revealed no difference in IL‐4 and IL‐5 mRNA levels between the OVA and OVA/RSV groups, and IL‐13 mRNA was significantly decreased in the OVA/RSV mice compared to the OVA group. Flow cytometric analysis of Type 2 cytokines demonstrated the same frequency of IL‐4 and IL‐5 production in lung‐derived T lymphocytes from the OVA/RSV and OVA groups. Direct cytokine ELISA measurements of lung supernatant showed the level of IL‐13 was significantly decreased in the OVA/RSV group compared to OVA mice, while there was no difference in either IL‐4 or IL‐5 between these two groups. These data indicate that the enhanced and prolonged AHR caused by the interaction of allergic airway inflammation and virus‐induced immune responses is a complex process that can not be explained simply by aug‐mented production of Type 2 cytokines. J. Med. Virol. 63:178–188, 2001. © 2001 Wiley‐Liss, Inc.
Bibliography:	ArticleID:JMV1013 istex:1395841764ACA5E1B54EAACC7F4147FC2719C451 ark:/67375/WNG-0Q0TH0R7-L ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0146-6615 1096-9071
DOI:	10.1002/1096-9071(20000201)63:2<178::AID-JMV1013>3.0.CO;2-O