OBJECTIVE Bronchopneumonia is a common respiratory infection disease and is the leading cause of hospitalization in children under 5 years of age. Inflammation is the primary response caused by bronchopneumonia. But the detailed underlying mechanism of inflammation in bronchopneumonia remains unclear. Therefore, this study focused on studying the effect of miR-216a-5p on inflammation induced by bronchopneumonia and investigate the potential mechanism underlying it. METHODS Human bronchial epithelial cells (BEAS-2B) were stimulated using lipopolysaccha-rides (LPS) to trigger bronchopneumonia in vitro. The production of interleukin (IL)-1β, IL-6, and Tumor necrosis factor (TNF)-α was measured using the enzyme-linked immunosorbent assay. The luciferase assay was conducted to explore the relationship between miR-216a-5p and TGFBR2. Quantitative real-time polymerase chain reaction and western blot were used to detect the gene expression. RESULTS miR-216a-5p gene expression decreased in BEAS-2B cells stimulated by LPS. Overexpression of miR-216a-5p suppressed the elevated levels of IL-1β, IL-6, and TNF-α induced by LPS. Transforming growth factor-beta receptor 2 (TGFBR2) proved to be a direct target of miR-216a-5p, and they negatively modulated TGFBR2 expression. In addition, overexpression of miR-216a-5p inhibited LPS-induced protein levels of TGFBR2,transforming growth factor (TGF)-β1, and phosphorylation of SMAD family member 2 (smad2),. This ectopic expression of miR-216a-5p was restored by overexpressed TGFBR2. CONCLUSION miR-216a-5p was decreased in LPS-stimulated BEAS-2B cells. Overexpressed miR-216a-5p suppressed LPS-induced inflammation in BEAS-2B cells by inhibition of TGF-β1 signaling via down-regulating TGFBR2. miR-216a-5p may be a valuable target for anti-inflammation treatment in bronchopneumonia.Bronchopneumonia is a common respiratory infection disease and is the main cause of hospitalization in children under 5 years of age. Inflammation is a primary response caused by bronchopneumonia. But the detailed underlying mechanism of inflammation in bronchopneumonia remains unclear. Therefore, this study focused on studying the effect of miR-216a-5p on inflammation caused by bronchopneumonia and investigate the potential mechanism underlying it. In this study, human bronchial epithelial cells (BEAS-2B) were stimulated using lipopolysaccharides (LPS) to trigger bronchopneumonia in vitro. miR-216a-5p was decreased in BEAS-2B cells stimulated by LPS. Overexpression of miR-216a-5p suppressed the elevated levels of interleukin (IL)-1β, IL-6, and Tumor necrosis factor (TNF)-α induced by LPS. Transforming growth factor-beta receptor 2 (TGFBR2) proved to be a direct target of miR-216a-5p, and they negatively modulated TGFBR2 expression. In addition, overexpression of miR-216a-5p inhibited LPS-induced protein levels of TGFBR2,transforming growth factor-beta 1 (TGF-β1), and phosphorylation of SMAD family member 2 (smad2. This ectopic overexpression of miR-216a-5p was restored by overexpressed TGFBR2. In conclusion, miR-216a-5p was decreased in LPS-stimulated BEAS-2B cells. Overexpressed miR-216a-5p suppressed LPS-induced inflammation in BEAS-2B cells by inhibition of TGF-β1 signaling via down-regulating TGFBR2. miR-216a-5p may be a valuable target for anti-inflammation treatment in bronchopneumonia.

中文翻译：

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MiR-216a-5p 通过下调 TGFBR2 抑制 TGF-β1 信号传导来减轻 LPS 诱导的人支气管上皮细胞炎症。

目的 支气管肺炎是一种常见的呼吸道感染性疾病，是 5 岁以下儿童住院的主要原因。炎症是由支气管肺炎引起的主要反应。但支气管肺炎炎症的详细潜在机制仍不清楚。因此，本研究重点研究miR-216a-5p对支气管肺炎诱导炎症的影响，并探讨其潜在机制。方法 使用脂多糖 (LPS) 刺激人支气管上皮细胞 (BEAS-2B) 在体外触发支气管肺炎。使用酶联免疫吸附测定法测量白细胞介素 (IL)-1β、IL-6 和肿瘤坏死因子 (TNF)-α 的产生。进行荧光素酶测定以探索miR-216a-5p与TGFBR2之间的关系。定量实时聚合酶链反应和蛋白质印迹用于检测基因表达。结果LPS刺激的BEAS-2B细胞中miR-216a-5p基因表达降低。miR-216a-5p 的过表达抑制了 LPS 诱导的 IL-1β、IL-6 和 TNF-α 水平升高。转化生长因子-β 受体 2 (TGFBR2) 被证明是 miR-216a-5p 的直接靶标，它们负向调节 TGFBR2 的表达。此外，过表达 miR-216a-5p 可抑制 LPS 诱导的 TGFBR2、转化生长因子 (TGF)-β1 和 SMAD 家族成员 2 (smad2) 的磷酸化水平。过表达的 TGFBR2 恢复了 miR-216a-5p 的这种异位表达。结论 miR-216a-5p 在 LPS 刺激的 BEAS-2B 细胞中降低。过表达的 miR-216a-5p 通过下调 TGFBR2 抑制 TGF-β1 信号传导来抑制 LPS 诱导的 BEAS-2B 细胞炎症。miR-216a-5p可能是支气管肺炎抗炎治疗的重要靶点。支气管肺炎是一种常见的呼吸道感染性疾病，是5岁以下儿童住院的主要原因。炎症是由支气管肺炎引起的主要反应。但支气管肺炎炎症的详细潜在机制仍不清楚。因此，本研究重点研究miR-216a-5p对支气管肺炎引起的炎症的影响，并探讨其潜在机制。在这项研究中，使用脂多糖 (LPS) 刺激人支气管上皮细胞 (BEAS-2B) 在体外触发支气管肺炎。LPS 刺激的 BEAS-2B 细胞中 miR-216a-5p 降低。miR-216a-5p 的过表达抑制了 LPS 诱导的白细胞介素 (IL)-1β、IL-6 和肿瘤坏死因子 (TNF)-α 水平升高。转化生长因子-β 受体 2 (TGFBR2) 被证明是 miR-216a-5p 的直接靶标，它们负向调节 TGFBR2 的表达。此外，miR-216a-5p 的过表达抑制 LPS 诱导的 TGFBR2、转化生长因子-β 1 (TGF-β1) 和 SMAD 家族成员 2 (smad2) 的磷酸化。miR-216a-5p 的这种异位过表达过表达的 TGFBR2 恢复。总之，LPS 刺激的 BEAS-2B 细胞中 miR-216a-5p 降低。过表达的 miR-216a-5p 通过抑制 TGF-β1 信号通路抑制 LPS 诱导的 BEAS-2B 细胞炎症-调节TGFBR2。