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EFFECTS OF ALLERGIC AIRWAYS DISEASE ON INFLUENZA VIRUS INFECTION IN BROWN NORWAY RATS
Citation:
Singh, P., D. W. Winsett, M. J. Daniels, J. Richards, C. A. Dick, K. B. Adler, AND M I. Gilmour. EFFECTS OF ALLERGIC AIRWAYS DISEASE ON INFLUENZA VIRUS INFECTION IN BROWN NORWAY RATS. Presented at American Thoracic Society, Atlanta, GA, May 17-22, 2002.
Description:
EFFECTS OF ALLERGIC AIRWAYS DISEASE ON INFLUENZA VIRUS INFECTION IN BROWN NORWAY RATS (P. Singhl, D.W. Winsett2, M.J. Daniels2,
C.A.J. Dick', K.B. Adlerl and M.I. Gilmour2, INCSU, Raleigh, N.C., 2NHEERL/ORD/ USEPA, RTP, N.C. and 3UNC, Chapel Hill, N.C.)The interaction between respiratory viral infections and allergic airways disease and asthma has been observed in both clinical settings and under experimental conditions. Increases in allergen-specific IgE titers have been reported in Brown Norway (BN) rats infected with rat-adapted influenza virus (RAI V) prior to allergic sensitization. In the present study, we investigate the effects of a preexisting allergic airways phenotype on susceptibility to influenza virus infection and its associated pathophysiology. Female BN rats were sensitized intratracheally (IT) with I0 g house dust mite (HDM) on days 1 and3. Two weeks later, rats were IT challenged with 10 g HDM followed by intranasal infection with 104 PFUs of RAIV, 24 hr later. Airway hyperresponsiveness (AHR) to inhaled methacholine (MCh) was assessed during peak viral titer (24 hr post infection) using a whole body plethysmograph, and lung injury and inflammation were assessed 24 and 48 hr post infection. RAIV-infected allergic rats demonstrated significantly greater AHR to MCh challenge when compared to both infected and non-infected, non-allergic rats as well as non-infected allergic rats. A sharp increase in total number of inflammatory cells with significant increases in eosinophils and lymphocytes was observed in the bronchoalveolar lavage fluid (BALF) of allergic, RAIV-infected rats. These rats also had significantly increased total IgE levels in BALF as well as increased cellular injury in the airways, evidenced by increases in lactate dehydrogenase and eosinophil peroxidase in BALF. We conclude that a preexisting allergic phenotype can exacerbate pathophysiological responses to influenza virus infection in the airways. (Supported by NCSU/EPA Training Agreement CT826512010.) (This abstract does not