Yang Guang, Zhou Xinyi, Chen Shutao, Liu Anfang, Liu Lingbin, Wang Haiwei, Wang Qigui, Lan Xi
College of Animal Science and Technology, Southwest University, Chongqing 400715, China.
Chongqing Academy of Animal Sciences, Chongqing 402460, China.
Animals (Basel). 2024 Feb 6;14(4):532. doi: 10.3390/ani14040532.
Prolonged exposure to high temperatures and humidity can trigger heat stress in animals, leading to subsequent immune suppression. Lipopolysaccharides (LPSs) act as upstream regulators closely linked to heat stress, contributing to their immunosuppressive effects. After an initial examination of transcriptome sequencing data from individual samples, 48 genes displaying interactions were found to potentially be associated with heat stress. Subsequently, to delve deeper into this association, we gathered chicken bone marrow dendritic cells (BMDCs). We combined heat stress with lipopolysaccharides and utilized a 48 × 48 Fluidigm IFC quantitative microarray to analyze the patterns of gene changes under various treatment conditions. The results of the study revealed that the combination of heat stress and LPSs in a coinfection led to reduced expressions of , , and . These differentially expressed genes triggered a pro-inflammatory response within cells via the MAPK and IL-17 signaling pathways. This response, in turn, affected the intensity and duration of inflammation when experiencing synergistic stimulation. Therefore, LPSs exacerbate the immunosuppressive effects of heat stress and prolong cellular adaptation to stress. The combination of heat stress and LPS stimulation induced a cellular inflammatory response through pathways involving cAMP, IL-17, MAPK, and others, consequently leading to decreased expression levels of , , and .
长时间暴露于高温和高湿度环境会引发动物的热应激反应，进而导致免疫抑制。脂多糖（LPS）作为与热应激密切相关的上游调节因子，促成了其免疫抑制作用。在初步检查单个样本的转录组测序数据后，发现48个显示相互作用的基因可能与热应激有关。随后，为了更深入地探究这种关联，我们收集了鸡骨髓树突状细胞（BMDC）。我们将热应激与脂多糖相结合，并使用48×48的Fluidigm IFC定量微阵列来分析不同处理条件下的基因变化模式。研究结果表明，热应激和LPS共同感染会导致[此处原文缺失具体基因名称]的表达降低。这些差异表达基因通过MAPK和IL - 17信号通路在细胞内引发促炎反应。反过来，这种反应在经历协同刺激时会影响炎症的强度和持续时间。因此，LPS会加剧热应激的免疫抑制作用，并延长细胞对应激的适应时间。热应激和LPS刺激的组合通过涉及cAMP、IL - 17、MAPK等的途径诱导细胞炎症反应，从而导致[此处原文缺失具体基因名称]的表达水平降低。
