| Background:In recent years, many studies indicate that viral respiratory infection has been associated with asthma. Asthma is a kind of chronic airway inflammation in nature. Our clinical investigation indicates that there is high incidence of Coxsackie virus B in respiratory infection and CVB infection maybe have role in acute asthma exacerbations, CVB commonly precede asthma in children. Our lab have established animal model of respiratory tract infection and airway hyperresponsiveness of CVB3. There are few studies about CVB inducing airway inflammation in the world. NF-κB, as one of the key molecular of complicate signal transduction pathways, regulates genes expression of immuno-response and expression of many inflammatory factors. NF-κB has been considered to play an important role in the process of asthma in recent researches . Objectives:In this study, the different airway inflammation in different infection status was observed, by establishing rats model of respiratory tract infection of CVB3. In further ,expression and activation of NF-κB in lungs of rats in respiratory tract infection of CVB3 is observed. Synchronously, expression of NF-κB in peripheral blood mononuclear cells of children suffered from asthma with CVB infection is observed in trial.Methods:1.Airway inflammation induced by CVB3: 35 Wistar rats were randomly divided into seven groups: control group (C, n=5), the ovalbumin sensitization group (OVA, n=6), the CVB3 infection groups which were divided into five groups, including two groups exposured to CVB3 once, 2w(V2w, n=5), 4w(V4w, n=5); one twice (V+V,n=6); two with ovalbumin sensitizations including intraperitoneally(V+OVA1, n=5), intranasally(V+OVA2, n=5). The CVB3 infection groups were infected by dropping CVB3 intranasally. Antibody of CVB3 was detected using indirect ELISA 14 days after infection. Rats of the group V+V and the group V+OVA were exposed to CVB3 again in 14th intranasally. Pathological changes were examined 14 days or 28 days after infection and infiltration of mast cell was examined using modified toluidine blue staining method. 2.Expression of NF-κB in lungs: 16 Wistar rats were randomly divided into two groups: control group (n=6), the CVB3 infection group(n=10), the CVB3 infection group was established by aerosolization with an ultrasonic nebulizer. Immunohistochemisty(IHC) was used to observed the expression of NF-κB in lungs 14 days after infection.3. Expression of NF-κB in PBMC of children with asthma: 12 inpatients, control group (n=3), the asthma without CVB infection group (n=4), the asthma with CVB infection group (n=5), Flow cytometry(FCM)was used to observed the expression of NF-κB in peripheral blood mononuclear cells 2 days after hospitalization.Results:1.Observation of airway inflammation: The OD of CVB3-IgM in the group of rats with virus infection (2w) was significantly higher than the control group (group V2w: 0.130±0.080, group C: 0.060±0.023, P<0.01). (1) Of the group V2w, the account of total inflammatory cells (320.850110.997) and mast cells (20.4508.268) was significantly higher than the group V4w(187.88017.074 and 7.4001.915), P<0.01. (2) Of the group V+V, the account of total inflammatory cells (298.93385.731) was significantly higher than the group V4w, P<0.01; but no significant difference compared with the group V2w. (3) Of the group V+OVA1 and the group V+OVA2 , the account of total inflammatory cells and mast cells was significantly higher than the group OVA(74. 9 00 28. 493 and 3. 4 2 93. 0 03), P<0.01,but there was no significant difference with each other(V+OVA1:201.88655.777 and 5.4002.327,V+OVA2:184.16043.828 and 7.0502.625). (4)Of the group OVA, the account of total inflammatory cells and mast cells was significantly lower than the group V4w,but significantly higher than that group C(34.86616.698 and 0.8670.516), P<0.01. (5)The account of total inflammatory cells was correlated with that of mast cells,r=0.80729, α=0.05. 2.Expression of NF-κB in lungs of rats and... |
PDF Full Text Request