Effects of sIL-13Rα2 combined with sIL-5R on Eosinophil apoptosis and Eotaxin levels in BALF of asthmatic mice

Chinese Journal of Asthma(2012)

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摘要
Objective To investigate the effects of soluble interleukin-13 receptor α2 (sIL-13Rα2)combined with soluble interleukin-5 receptor (sIL-5R) on the apoptosis of Eosinophils and Eotaxin levels in bronchoalveolar lavage fluid (BALF) of asthmatic mice and explore possible mechanisms of treating asthmatic mice with them.Methods Fifty BALB/c mice were randomly divided into five groups:naive mice,saline sham treated mice,sIL-13Rα2 treated mice,sIL-5R treated mice and sIL-13Rα2 combined with sIL-5R treated mice (combination treated mice).Animals were actively sensitized by intraperitoneal injection of ovalbumin (OVA).Mice in the latter 3 groups,30 min before challenged,were respectively injected intraperitoneally with sIL-13Rα2 100 μg,sIL-5R 100 μg and sIL-13Rα2 100 μg plus sIL- 5R100 μg.Naive mice and saline sham treated mice received equal volume of saline. The apoptotic ratios were analyzed by flow cytometry (FCM). The levels of Eotaxin were detected by enzyme-linked immunosorbent assay (ELISA).Results ①In saline sham treated mice,the ratios of Eosinophils and Eotaxin levels in BALF were remarkably higher than that in naive mice (all P <0.01),and the apoptotic ratios (AR) obviously lower (P <0.01).②Compared with saline sham treated mice,the ratios of Eosinophils and Eotaxin levels significantly decreased in sIL-13Rα2 treated mice,sIL-5R treated mice and combination treated mice (all P <0.01),and the apoptotic ratios (AR) obviously increased ( P <0.05).③Compared with single treatment,combined treatment were more effective ( P <0.05).Conclusions These results indicate that combination sIL-13Rα2 with sIL-5R could more promote apoptosis of Eosinophils and lower the levels of Eotaxin than their sole effects,and more efficiently relieve airway inflammation.Our findings suggest that combined treatment with these molecular targets could be a useful therapeutic strategy for asthma. Key words: Asthma ;  Soluble interleukin-13 receptor α2; Soluble interleukin-5 receptor; Apoptosis; Eotaxin
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