Objective To investigate the role of endogenous Hydrogen Sulfide ( H2S) in airway inflammation and responsiveness in a rat model of chronic passive-smoking. Methods Male SD rats were randomly divided into a control group ( breathing fresh air) and a passive smoking group [ cigarette smoking( CS) passively] , with 18 rats in each group. Six rats in each group were randomly intraperitoneally injected with normal saline, sodium hydrosulfide ( NaHS) or propargylglycine ( PPG, an irreversible inhibitor of cystathionine- γ-lyase) . The animals were divided into six subgroups, ie. Con group, NaHS group, and PPG group, CS group, CS+ NaHS group, and CS + PPG group. After 4 months, lung histological change and airway tension were measured. The H2S levels of plasma and lung tissue were analyzed by the sensitive sulphur electrode assay. The expression of cystathionine-γ-lyase ( CSE) was measured by western blot. Results Compared with the Con group, CSE protein expression in lung tissues was increased in CS group( P lt;0. 05) ; the H2 S levels of plasma were significantly higher in CS group, NaHS group and CS + NaHS group, and much lower in PPG group ( P lt; 0. 05, respectively) . Compared with CS group, the H2S levels of plasma were significantly higher in CS + NaHS group, and much lower in CS + PPG group( P lt; 0. 05, respectively) . The H2S level of lung tissue in each group had no significant difference ( P gt; 0. 05) . Compared with Con group,score of lung pathology was significant elevated, and the responsiveness of airway smooth muscles to ACh and KCl was significant augmented in CS group. Compared with CS group, the score of lung pathology was decreased, and the responsiveness of airway smooth muscles was decreased in CS +NaHS group( P lt;0. 05) , and vise versa in CS + PPG group( P lt; 0. 01) . Conclusion H2S can alleviate airway inflammation and hyperresponsiveness induced by CS, and administration of H2S might be of clinical benefit in airwayinflammation and airway responsiveness.
Objective To study the concentration of neurotrophins( including NGF, BDNF, NT3 and NT4) in the lung of SD rats infected by respiratory syncytial virus( RSV) , and to explore the relationship between the concentration of the neurotrophins, airway hyperresponsiveness and airway neural plasticity.Methods Twenty SD newborn rats were randomly divided into a control group and a RSV-infected group with ten rats in each group. The RSV-infected group were infected with 5 ×104 TCID50/0. 1 mL RSV each week. After 8 weeks, the bronchial responsiveness of the SD rats was assessed. The bronchial inflammation was assessed by HE staining with left lung. Synaptophysin and neurofilament expressions in the lung of SD rats were assayed by the immunohistochemistry staining. In situ hybridization was used to detect the RSV RNA in the lung. The concentration of neurotrophins in the lung of SD rats were detected by ELISA. Results The RSV-infected group showed elevated airway hyperresponsiveness and more inflammatory cells infiltrated in the lung; In situ hybridization showed positive signal of RSV RNA in lung interstitium of the RSV-infected rats. Synaptophysin and neurofilame levels in the airway were increased in the RSV-infected group. Supernatant levels of NGF and BDNF were significantly increased compared with the control group ( P lt;0. 05) . The NT3 and NT4 levels had no significant difference in all groups. The expressions of NGF and BDNF were positively related to the expressions of synaptophysin( r1 = 0. 892, r2 = 0. 995, P lt; 0. 05) and neurofilament( r1 = 0. 949, r2 =0. 936, P lt;0. 05) , also positively related to the airway hyperresponsiveness ( r1 =0. 929, r2 = 0. 910, P lt; 0. 05) . Conclusion RSV infection results in increased expressions of NGF and BDNF in the lung, which are correlated to the change of airway neural plasticity and airway hyperresponsiveness.
ObjectiveTo explore the effects of Aspergillus fumigatus (A. fumigatus) on airway inflammation, airway responsiveness and total serum IgE in asthmatic rats. MethodsEighteen male Wistar rats were divided into three groups randomly, ie. a normal control group, an asthmatic model group, and an A. fumigatus group. The rats in the model group and the A.fumigatus group were sensititized and challenged with ovalbumin to establish asthmatic model. After establishment of asthmatic model, the rats in the A. fumigatus group were treated with chronic A. fumigatus spores inhalation. Subsequently, airway responsiveness/sensitivity to methacholine(Ach), levels of serum IgE and airway inflammation were assessed and compared among three groups. ResultsCompared with the asthmatic rats, the rats treated with A. fumigatus showed higher airway responsiveness (Penh/baselin value was significantly increased at the Mch concentration of 12.5, 25 and 50 mg/mL), increased inflammatory cells infiltration in pulmonary tissue slices and increased serum IgE level (P < 0.05). Most importantly, serum IgE level was detected in close relationship with PC100 which was defined as the dose of Mch causing 100% increase of enhance pause (Penh) value without Mch challenge (r=-0.873, P < 0.01). Serum IgE level was also closely related to the percentage of eosinophils in bronchoalveolar lavage fluid (r=0.937, P < 0.01). ConclusionsChronic A. fumigatus inhalation aggravates airway inflammation, bronchial hyperresponsiveness and serum IgE level in asthma. IgE may play an important role in facilitating the development of bronchial responsiveness and eosinophilic inflammation.