Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:Early-life viral infection and allergen exposure interact to induce an asthmatic phenotype in mice. | Siegle et al. Respiratory Research 2010 11 14 http content 11 1 14 RESPIRATORY RESEARCH RESEARCH Open Access Early-life viral infection and allergen exposure interact to induce an asthmatic phenotype in mice I - r r i - - c Ci S z t I 1 l I I I I_I m r Pk 2 31 r I r f- U . I_I r p r f- 1 I_I I z v z c D z r Y r i4 I z r p D z m z z t A If l Z 5 Jessica S Siegle Nicole Hansbro Cristan Herbert Helene F Rosenberg Joseph B DomachowsKe Kelly L Asquith2 3 Paul S Foster2 3 RaKesh K Kumar1 Abstract Background Early-life respiratory viral infections notably with respiratory syncytial virus RSV increase the risk of subsequent development of childhood asthma. The purpose of this study was to assess whether early-life infection with a species-specific model of RSV and subsequent allergen exposure predisposed to the development of features of asthma. Methods We employed a unique combination of animal models in which BALB c mice were neonatally infected with pneumonia virus of mice PVM which replicates severe RSV disease in human infants and following recovery were intranasally sensitised with ovalbumin. Animals received low-level challenge with aerosolised antigen for 4 weeks to elicit changes of chronic asthma followed by a single moderate-level challenge to induce an exacerbation of inflammation. We then assessed airway inflammation epithelial changes characteristic of remodelling airway hyperresponsiveness AHR and host immunological responses. Results Allergic airway inflammation including recruitment of eosinophils was prominent only in animals that had recovered from neonatal infection with PVM and then been sensitised and chronically challenged with antigen. Furthermore only these mice exhibited an augmented Th2-biased immune response including elevated serum levels of anti-ovalbumin IgE and IgG1 as well as increased relative expression of Th2-associated cytokines IL-4 IL-5 and IL-13. By comparison development of AHR and mucous cell change were .
