Characterization of autophagy and immune cell infiltration in bronchopulmonary dysplasia: a bioinformatics analysis
10.3760/cma.j.cn113903-20240819-00574
- VernacularTitle:支气管肺发育不良中自噬和免疫细胞浸润的特征：生物信息学分析
- Author:
Wei WEI
1
;
Chao LIU
1
;
Shenglin PEI
1
Author Information
1. 广西医科大学附属肿瘤医院（广西壮族自治区肿瘤防治研究所）麻醉科，南宁 530021
- Publication Type:Journal Article
- Keywords:
Bronchopulmonary dysplasia;
Autophagy;
Immune cell infiltration;
Bioinformatics
- From:
Chinese Journal of Perinatal Medicine
2025;28(6):452-459
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To characterize autophagy dysregulation and immune cell infiltration in bronchopulmonary dysplasia (BPD) and identify potential therapeutic targets for clinical intervention.Methods:Gene expression profiles of BPD and an autophagy-related gene list were obtained from the Gene Expression Omnibus and Human Autophagy Database. Raw data were processed using bioinformatics approaches to identify differentially expressed genes (DEGs), followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. A protein-protein interaction (PPI) network was constructed to screen hub autophagy genes and the expression levels were validated in a BPD animal model through animal experiments. Drug-target prediction of autophagy-related genes was performed using network analysis, and immune infiltration features in BPD were analyzed by ssGSEA and CIBERSORT algorithms. Statistical significance was assessed via two-sample t-tests. Results:We identified 4 866 DEGs in BPD, including 61 autophagy-related genes enriched in macroautophagy and autophagy regulation pathways. PPI analysis revealed ten hub genes, including PARP1, HSP90AB1, and PTEN, with downregulated expression in BPD animal model. The expression levels of PARP1, HSP90AB1, and PTEN in the BPD mice were all lower than those in the control group (0.33±0.07 vs. 0.66±0.15, t=3.54; 0.46±0.41 vs. 1.45±0.33, t=3.39; 0.72±0.19 vs. 1.25±0.25; t=2.91; all P<0.05). Drug-target prediction highlighted N-acetyl-L-cysteine, vorinostat, and sorafenib as potential therapies. Immune profiling demonstrated significant shifts in naive B cells, memory B cells, CD8 +T cells, and neutrophils, indicating a pro-inflammatory and immunosuppressive microenvironment. Conclusions:Autophagy-immune axis dysregulation may contribute to BPD pathogenesis. The aberrant expression of PARP1, HSP90AB1, and PTEN provides novel mechanistic insights into BPD, while identified drug candidates targeting autophagy genes offer translational potential for BPD treatment.
