Abstract：
BACKGROUND: Infantile pneumonia is an acute inflammatory lesion of the lung caused by mycoplasma pneumonia. Indeed, Twist2 signaling pathway controls inflammatory reaction, oxidative stress, and other biological reaction. However, the regulation of Twist2 on the inflammation in infantile pneumonia remains unclear. This study explained that the function and mechanism of Twist2 in infantile pneumonia.
METHODS: The subjects included the serum samples of 12 patients with infantile pneumonia and normal healthy volunteers from Hunan Children\'s Hospital. Besides, mice were given with lipopolysaccharide (LPS) into the lung. Moreover, RAW264.7 macrophages were stimulated with LPS for 4 h and added to the culture medium.
RESULTS: In present study, in serum of patients with infantile pneumonia or lung tissue of mice model with infantile pneumonia, TWIST2 expression was lessened. Apart from that, TWIST2 protein could reduce the inflammatory reaction in mice model with infantile pneumonia, resulting in an inhibition in lung injury. Conversely, over-expression of TWIST2 also decreased inflammatory reaction in macrophages model via the regulation of FOXO1/NLRP3 pathway. Downregulation of TWIST2 promoted the inflammation in macrophages model by the regulation of FOXO1/NLRP3 pathway.
CONCLUSIONS: According to the findings, present study have identified that the TWIST2 could reduce the inflammation of infantile pneumonia by NLRP3 inflammasome through the regulation of mitochondrial permeability transition and the induction of FOXO1 expression.
METHODS: The subjects included the serum samples of 12 patients with infantile pneumonia and normal healthy volunteers from Hunan Children\'s Hospital. Besides, mice were given with lipopolysaccharide (LPS) into the lung. Moreover, RAW264.7 macrophages were stimulated with LPS for 4 h and added to the culture medium.
RESULTS: In present study, in serum of patients with infantile pneumonia or lung tissue of mice model with infantile pneumonia, TWIST2 expression was lessened. Apart from that, TWIST2 protein could reduce the inflammatory reaction in mice model with infantile pneumonia, resulting in an inhibition in lung injury. Conversely, over-expression of TWIST2 also decreased inflammatory reaction in macrophages model via the regulation of FOXO1/NLRP3 pathway. Downregulation of TWIST2 promoted the inflammation in macrophages model by the regulation of FOXO1/NLRP3 pathway.
CONCLUSIONS: According to the findings, present study have identified that the TWIST2 could reduce the inflammation of infantile pneumonia by NLRP3 inflammasome through the regulation of mitochondrial permeability transition and the induction of FOXO1 expression.
摘要：
背景：小儿肺炎是由支原体肺炎引起的肺部急性炎性病变。的确,Twist2信号通路控制炎症反应，氧化应激，和其他生物反应。然而,Twist2对小儿肺炎炎症的调节尚不清楚.本研讨解释Twist2在小儿肺炎中的功效和机制。
方法：研究对象包括湖南省儿童医院12例小儿肺炎患者和正常健康志愿者的血清标本。此外,小鼠肺部给予脂多糖(LPS)。此外，用LPS刺激RAW264.7巨噬细胞4小时并加入到培养基中。
结果：在本研究中，在小儿肺炎患者血清或小儿肺炎模型小鼠肺组织中,TWIST2表达减少。除此之外,TWIST2蛋白能减轻小儿肺炎模型小鼠的炎症反应,导致肺损伤的抑制。相反，TWIST2的过表达还通过调节FOXO1/NLRP3通路降低了巨噬细胞模型的炎症反应。TWIST2下调通过调节FOXO1/NLRP3通路促进巨噬细胞模型的炎症反应。
结论：根据调查结果，目前研究发现TWIST2可以通过调节线粒体通透性转换和诱导FOXO1表达来减轻NLRP3炎症小体对小儿肺炎的炎症反应。
方法：研究对象包括湖南省儿童医院12例小儿肺炎患者和正常健康志愿者的血清标本。此外,小鼠肺部给予脂多糖(LPS)。此外，用LPS刺激RAW264.7巨噬细胞4小时并加入到培养基中。
结果：在本研究中，在小儿肺炎患者血清或小儿肺炎模型小鼠肺组织中,TWIST2表达减少。除此之外,TWIST2蛋白能减轻小儿肺炎模型小鼠的炎症反应,导致肺损伤的抑制。相反，TWIST2的过表达还通过调节FOXO1/NLRP3通路降低了巨噬细胞模型的炎症反应。TWIST2下调通过调节FOXO1/NLRP3通路促进巨噬细胞模型的炎症反应。
结论：根据调查结果，目前研究发现TWIST2可以通过调节线粒体通透性转换和诱导FOXO1表达来减轻NLRP3炎症小体对小儿肺炎的炎症反应。
