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Updated: Oct 2, 2026
Modeling Dysplastic and Functional Lung Alveolar Repair after Influenza Infection
Published on: September 19, 2025
Correlative changes of interferon-gamma and interleukin-4 between cortical layer and pulmonary airway of sensitized
Qiang-Min Xie1, Ji-Qiang Chen, Wen-Hui Shen
1Zhejiang Respiratory Drugs Research Laboratory of State Drugs Administration of China, Medical School of Zhejiang University, Hangzhou 310031, China. Xieqm@zju.edu.cn
Aim:
To explore correlation of T helper 1 (Th1) and Th2 cytokine between the cortical layer and pulmonary airway in ovalbumin-induced rat asthma model.
Methods:
Aerosol antigen-induced changes of inflammation in bronchoalveolar lavage fluids (BALF) and pulmonary histologic section in sensitized rats were investigated. Changes of interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) in BALF and cortical layer homogenates were determined by ELISA.
Results:
The number of inflammatory cells in BALF in antigen challenged group was significantly higher than control group (P <0.05). Dexamethasone (DXM, 0.5 mg/kg, ip) markedly reduce total leukocyte numbers in BALF, and almost completely inhibited eosinophil, lymphocyte accumulation. The score of histological examination (eosinophil infiltration, mucous edema and epithelial lesion) in antigen challenged group was significantly higher than control group (P <0.05). DXM (0.5 mg/kg, ip) reduced the numbers of eosinophils and improved mucous edema and epithelial lesion of bronchi and bronchioles. In addition, our results demonstrated decreased IFN-gamma level accompanied by increased IL-4 level that resulted in a decreased IFN-gamma/IL-4 ratio in the BALF after the sensitized rats were challenged with aerosol antigen. Meanwhile, there was a similar change of IFN-gamma and IL-4 in cortical layer homogenates. DXM (0.5 mg/kg, ip) could reverse IFN-gamma/IL-4 ratio in the BALF and cortical layer homogenates in the model.
Conclusion:
The results showed a significant interplay changes of Th1 and Th2 cytokine between central nervous system and pulmonary airway in the asthmatic inflammatory model.
