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Characterization of an acute influenza infection in a murine model of allergic asthma and responses to corticosteroid

Respiratory viruses affect many aspects of asthma including the responsiveness to corticosteroids. Underlying mechanisms still needs to be elucidated. An interplay between viral respiratory infection and allergic airway inflammation and corticosteroid effectivenesswere investigated in murine Influenza A virus infection (Puerto Rico/8/1934 (H1N1)combined with ovalbumin (OVA) exposure in allergen-sensitized host. BALB/c mice were intraperitoneally sensitized with OVA on days 1 and 14. On day 16, mice were intranasally (IN) infected with H1N1. On day 20, mice were orally treated with dexamethasone (DEX) and challenged IN with OVA. On day 21, airway resistance and compliance were recorded (DSI's Buxco®) to assess airway hyperresponsiveness(AHR) to aerosolized methacholine. Cell counts in bronhoalveolar lavage fluid (BALF) and lung viral load were determined. In H1N1-infected asthmatic mice a significant increase in neutrophil, lymphocyte and macrophage count in BALF and increased AHR were observed. Treatment with DEX further exacerbated AHR and did not reduce neutrophil and lymphocyte counts in BALF. Partial reduction of eosinophil and macrophage counts and decrease in IP-10 and MCP-1 concentrations in BALF were observed following DEX treatment whilst lung viral load was not affected. In non-infected asthmatic mice DEX reduced eosinophil count, IL-4 and IL-5 levels in BALF and almost completely inhibited AHR. Conclusions: H1N1-associated OVA asthma exacerbation in mice was characterized by aggravation of the allergic airway inflammation, increased AHR and a shift towards selective insensitivity to corticosteroid treatment.

animal models , bronchoalveolar lavage , lung function testing

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