| Purpose: Respiratory virus infection is one of the most critical factorsinducing the exacerbation of asthma. Respiratory syncytial virus (RSV) is oneof major viruses provoking lower respiratory infection of infants and childrenin fall and winter and it is known to lead to the infiltration of eosinophil intothe bronchus by increasing the production of chemokines such as macrophageinflammatory protein-1alpha (MIP-1α) and regulated on activation, normalT-cells expressed and secreted (RANTES). However, there have been only afew studies on the difference in RANTES production between children withasthma and normal ones for RSV infection. Therefore, this study investigatedthe difference in RANTES production between asthma mice and control miceafter RSV infection in a murine model of asthma.Methods: A murine model of asthma was made by sensitizing BALB/cmice with Dermatophagoides farinae（Der f）, an antigen of house dust mite.After infecting the murine model of asthma with RSV, the concentration ofRANTES in bronchoalveolar lavage fluid (BALF) was measured. In addition,airway resistance, the number of inflammatory cells in BALF and interferon–gamma level after the viral infection were examined.Results: Although both of mice with asthma and mice of the controlgroup showed increased RANTES production after RSV infection, thedifference between the two groups was not significant. When asthma mice werecompared before and after RSV infection, airway resistance became higher andthe number of eosinophil was not changed but the number of neutrophil wasincreased. The interferon-gamma level was not raised by RSV infection inboth of the asthma and the control groups. Conclusions: This study found that RSV infection did not lead to moreRANTES production in asthma mice compared to mice of the control group.This finding implies that RSV infection induces RANTES productionregardless of asthma and asthma patients do not show acute exacerbationthrough increased RANTE production. |
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