Identification of candidate aberrant differentially methylated/expressed genes in asthma.

BACKGROUND: Asthma is an important non-communicable disease worldwide. DNA methylation is associated with the occurrence and development of asthma. We are aimed at assuring differential expressed genes (DEGs) modified by aberrantly methylated genes (DMGs) and pathways related to asthma by integrating bioinformatics analysis. METHODS: One mRNA dataset (GSE64913) and one gene methylation dataset (GSE137716) were selected from the Gene Expression Omnibus (GEO) database. Functional enrichment analysis was performed using GeneCodies 4.0 database. All gene expression matrices were analyzed by Gene set enrichment analysis (GSEA) software. STRING was applied to construct a protein-protein interaction (PPI) network to find the hub genes. Then, electronic validation was performed to verify the hub genes, followed by the evaluation of diagnostic value. Eventually, quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to detect the expression of hub genes. RESULTS: In total, 14 hypomethylated/high-expression genes and 10 hypermethylated/low-expression genes were obtained in asthma. Among them, 10 hub genes were identified in the PPI network. Functional analysis demonstrated that the differentially methylated/expressed genes were primarily associated with the lung development, cytosol and protein binding. Notably, HLA-DOA was enriched in asthma. FKBP5, WNT5A, TM4SF1, PDK4, EPAS1 and GMPR had potential diagnostic value for asthma. CONCLUSION: The project explored the pathogenesis of asthma, which may provide a research basis for the prediction and the drug development of asthma.

[Effects of smoke inhalation injury on the phagocytic function of rat alveolar macrophage and on neutrophil apoptosis].

OBJECTIVE: To investigate the effects of smoke inhalation injury on the phagocytic function of rat alveolar macrophages and neutrophil apoptosis. METHODS: Wistar rats inflicted with smoke inhalation injury were employed in the study. Fifty-four Wistar rats were randomly divided into normal control (N, n = 6) and inhalation injury (I, n = 48) groups. Alveolar macrophages were harvested from the BALF (bronchoalveolar lavage fluid) in I group of rats at 2, 6, 12 and 24 postburn hours (PBHs) and on 2, 3, 4 and 5 postburn days (PBDs). The dynamic change in the phagocytosis of chicken erythrocytes by alveolar macrophages in vitro was observed. The positive rate of myeloperoxidase (MPO) staining of alveolar macrophages (AMs) by MPO staining method was observed, so as to indirectly reflect neutrophil apoptosis and the phagocytosis o apoptotic neutrophils by AMs. Furthermore, the dynamic change in the inflammatory cell apoptosis within BALF was monitored by flow cytometry. RESULTS: (1) he phagocytosis of chicken erythrocytes by AMs was decreased during early postburn stage (2 - 6 PBHs) but recovered after 12 PBHs. (2) The positive MPO staining of AMs was increased gradually after injury and reached top level at 24 PBHs, but decreased during 2 - 5 PBDs. (3) The apoptotic rate within BALF was around 3.02% - 12.95% and rose to peak value at 24 PBHs. CONCLUSION: There was increased apoptosis of inflammatory cells within BALF. The resolution process of inflammation after smoke inhalation injury involved neutrophil apoptosis and the phagocytosis of apoptotic neutrophils by AMs.

[The change in apoptosis and proliferation of pulmonary tissue cells in rats with smoke inhalation injury].

OBJECTIVE: To observe the rule of the change of apoptosis and proliferation of pulmonary tissue cells in rats with inhalation injury, so as to explore the significance of apoptosis in the repairing process of pulmonary tissue injury. METHODS: Smoke inhalation injury model was established in rats. The rats were randomly divided into normal control (NC) and smoke inhalation injury (SI) groups. TUNEL and immunohistochemistry methods were employed to determine the changes in cellular apoptotic and proliferating cell nuclear antigen (PCNA) indices of the pulmonary tissue at different postburn time points. RESULTS: (1) The apoptotic index increased at 2 postburn hours (PBHs) and remained at high levels thereafter. (2) The PCNA index increased at 12 PBHs, reaching top level at 3 postburn days (PBDs), remaining kept at relativly high level later. CONCLUSION: Apoptosis not only played roles in the early pulmonary injury after smoke inhalation injury, but also participated in the repair and modification of the proliferated tissue during later reconstruction.