1.The number of FOXP3+regulatory T cells (Tregs) decreased and transformed into RORγt+FOXP3+Tregs in lung tissues of mice with bronchopulmonary dysplasia.
Langyue HE ; Hongyan LU ; Ying ZHU ; Jianfeng JIANG ; Huimin JU ; Yu QIAO ; Shanjie WEI
Chinese Journal of Cellular and Molecular Immunology 2024;40(1):7-12
Objective To explore the phenotypic conversion of regulatory T cells (Tregs) in the lungs of mice with bronchopulmonary dysplasia (BPD)-affected mice. Methods A total of 20 newborn C57BL/6 mice were divided into air group and hyperoxia group, with 10 mice in each group. The BPD model was established by exposing the newborn mice to hyperoxia. Lung tissues from five mice in each group were collected on postnatal days 7 and 14, respectively. Histopathological changes of the lung tissues was detected by HE staining. The expression level of surfactant protein C (SP-C) in the lung tissues was examined by Western blot analysis. Flow cytometry was performed to assess the proportion of FOXP3+ Tregs and RORγt+FOXP3+ Tregs in CD4+ lymphocytes. The concentrations of interleukin-17A (IL-17A) and IL-6 in lung homogenate were measured by using ELISA. Spearman correlation analysis was used to analyze the correlation between FOXP3+Treg and the expression of SP-C and the correlation between RORγt+FOXP3+ Tregs and the content of IL-17A and IL-6. Results The hyperoxia group exhibited significantly decreased levels of SP-C and radical alveolar counts in comparison to the control group. The proportion of FOXP3+Tregs was reduced and that of RORγt+FOXP3+Tregs was increased. IL-17A and IL-6 concentrations were significantly increased. SP-C was positively correlated with the expression level of RORγt+FOXP3+ Tregs. RORγt+FOXP3+ Tregs and IL-17A and IL-6 concentrations were also positively correlated. Conclusion The number of FOXP3+ Tregs in lung tissue of BPD mice is decreased and converted to RORγt+ FOXP3+ Tregs, which may be involved in hyperoxy-induced lung injury.
Animals
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Mice
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Mice, Inbred C57BL
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Bronchopulmonary Dysplasia
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T-Lymphocytes, Regulatory
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Interleukin-17
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Nuclear Receptor Subfamily 1, Group F, Member 3
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Hyperoxia
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Interleukin-6
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Forkhead Transcription Factors
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Lung