Hainan Key Laboratory of Tropical Animal Reproduction & Breeding and Epidemic Disease Research, Engineering Key Laboratory of Haikou, School of Animal Science and Technology, Hainan University, Haikou 570228, China.
Int J Mol Sci. 2023 Jan 9;24(2):1312. doi: 10.3390/ijms24021312.
can cause goat hemorrhagic sepsis and endemic pneumonia. Respiratory epithelial cells are the first line of defense in the lungs during infection. These cells act as a mechanical barrier and activate immune response to protect against invading pathogenic microorganisms. Upon infection, adheres to the cells and causes changes in cell morphology and transcriptome. ATAC-seq was conducted to determine the changes in the chromatin open region of -infected goat bronchial epithelial cells based on transcriptional regulation. A total of 13,079 and 28,722 peaks were identified in the control (CK) and treatment (T) groups (P. multocida infection group), respectively. The peaks significantly increased after infection. The specific peaks for the CK and T groups were annotated to 545 and 6632 genes, respectively. KEGG pathway enrichment analysis revealed that the specific peak-related genes in the T group were enriched in immune reaction-related pathways, such as Fc gamma R-mediated phagocytosis, MAPK signaling pathway, bacterial invasion of epithelial cells, endocytosis, and autophagy pathways. Other cellular component pathways were also enriched, including the regulation of actin cytoskeleton, adherent junction, tight junction, and focal adhesion. The differential peaks between the two groups were subsequently analyzed. Compared to those in the CK group, 863 and 11 peaks were upregulated and downregulated, respectively, after the infection. Fifty-six known transcription factor motifs were revealed in upregulated peaks in the -infected group. By integrating ATAC-seq and RNA-seq, some candidate genes (SETBP1, RASGEF1B, CREB5, IRF5, TNF, CD70) that might be involved in the goat bronchial epithelial cell immune reaction to infection were identified. Overall, infection changed the structure of the cell and caused chromatin open regions to be upregulated. In addition, infection actively mobilized the host immune response with the inflammatory phenotype. The findings provide valuable information for understanding the regulatory mechanisms of -infected goat bronchial epithelial cells.
可引起山羊出血性败血症和地方性肺炎。呼吸道上皮细胞是肺部感染时的第一道防线。这些细胞作为机械屏障并激活免疫反应，以防止入侵的致病微生物。感染后，附着在细胞上，引起细胞形态和转录组的变化。ATAC-seq 用于根据转录调控确定感染山羊支气管上皮细胞后染色质开放区域的变化。在对照 (CK) 和处理 (T) 组 (多杀性巴氏杆菌感染组) 中分别鉴定出 13079 和 28722 个峰。感染后，峰显著增加。CK 和 T 组的特定峰分别注释到 545 和 6632 个基因。KEGG 途径富集分析表明，T 组中特定峰相关基因富集于免疫反应相关途径，如 Fc γ R 介导的吞噬作用、MAPK 信号通路、上皮细胞细菌入侵、内吞作用和自噬途径。其他细胞成分途径也被富集，包括肌动蛋白细胞骨架的调节、黏着连接、紧密连接和焦点附着。随后分析了两组之间的差异峰。与 CK 组相比，感染后分别有 863 个和 11 个峰上调和下调。在感染组的上调峰中揭示了 56 个已知的转录因子基序。通过整合 ATAC-seq 和 RNA-seq，鉴定了一些可能参与山羊支气管上皮细胞对感染免疫反应的候选基因 (SETBP1、RASGEF1B、CREB5、IRF5、TNF、CD70)。总的来说，感染改变了细胞的结构，导致染色质开放区域上调。此外，感染积极调动宿主免疫反应，表现为炎症表型。研究结果为了解感染山羊支气管上皮细胞的调控机制提供了有价值的信息。
