Abstract:Objective To explore the impact of nuclear factor-κB p65 (NF-κB p65) on the apoptosis of alveolar epithelial cells induced by Streptococcus pneumoniae and the expression of inflammatory cytokines. Methods Alveolar epithelial cells were divided into the control group, the infection group, the interference group and the negative control (NC) group. The infection group, the interference group and the NC group were treated with Streptococcus pneumoniae. The interference group and the NC group were transfected with siRNA NF-κB p65 and siRNA control respectively, while the control group was not treated. ELISA assay was used to detect the levels of IL-10 and IL-6 in cell culture supernatant, flow cytometry to detect cell apoptosis, RT-PCR to detect NF-κB p65 level in cells, and Western blot to detect Cleaved Caspase-3 and Bcl-2-associated X protein (Bax) levels in cells. Results The levels of NF-κB p65, IL-6, Cleaved Caspase-3 and Bax and the cell apoptosis rate were all significantly higher in the infection group and the NC group than in the control group, while the level of IL-10 was significantly lower in the above-mentioned two groups than in the control group (P<0.01). Compared with the infection group, the levels of NF-κB p65, IL-6, Cleaved Caspase-3 and Bax and the cell apoptosis rate were all significantly lower in the interference group (all P<0.01), while the level of IL-10 was significantly higher in the interference group (P<0.01). Conclusions NF-κB p65 can inhibit the apoptosis of alveolar epithelial cells induced by Streptococcus pneumoniae and the expression of inflammatory cytokines, and its mechanism may be related to the levels of Cleaved Caspase-3 and Bax .
王勇, 孙朝峰, 胡钱红. NF-κBp65对肺炎链球菌诱导的肺泡上皮细胞凋亡及炎性因子表达的影响[J]. 实用预防医学, 2018, 25(5): 547-550.
WANG Yong, SUN Zhao-feng, HU Qian-hong. Effect of NF-κB p65 on apoptosis of alveolar epithelial cells induced by Streptococcus pneumoniae and expression of inflammatory cytokines. , 2018, 25(5): 547-550.
[1] Maier BB, Hladik A, Lakovits K, et al. Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice[J]. Euro J Immunol, 2016, 46(9):2175-2186. [2] Walters KA, D'agnillo F, Sheng ZM, et al. 1918 pandemic influenza virus and Streptococcus pneumoniae co-infection results in activation of coagulation and widespread pulmonary thrombosis in mice and humans[J]. J Pathol, 2016, 238(1):85-97.[3] Dong S, Zhong Y, Lu W, et al. Baicalin inhibits lipopolysaccharide-induced inflammation through signaling NF-κB pathway in HBE16 airway epithelial cells[J]. Inflammation, 2015, 38(4):1493-1501. [4] Relja B, Omid N, Wagner N, et al. Ethanol, ethyl and sodium pyruvate decrease the inflammatory responses of human lung epithelial cells via Akt and NF-κB in vitro but have a low impact on hepatocellular cells[J]. Int J Mol Med, 2016, 37(2):517-525. [5] Jing W, Chunhua M, Shumin W. Effects of acteoside on lipopolysaccharide-induced inflammation in acute lung injury via regulation of NF-κB pathway in vivo and in vitro[J]. Toxicol Appl Pharmacol, 2015, 285(2):128-135. [6] 胡根. NF-κB/p65 基因在 TNF-α 诱导肺泡上皮细胞凋亡中的作用及可能机制[D].广州:南方医科大学, 2010. [7] 石榴, 李理, 袁伟锋, 等. RNAi 沉默 NF-κB p65 对小鼠巨噬细胞细胞因子表达的影响[J]. 中国病理生理杂志, 2011, 27(7):1264-1269. [8] Hou J, Wang T, Xie Q, et al. N-Myc-interacting protein (NMI) negatively regulates epithelial-mesenchymal transition by inhibiting the acetylation of NF-κB/p65[J].Cancer Lett, 2016, 376(1):22-33. [9] Sau A, Lau R, Cabrita MA, et al. Persistent activation of NF-κB in BRCA1-deficient mammary progenitors drives aberrant proliferation and accumulation of DNA damage[J]. Cell Stem Cell, 2016, 19(1):52-65. [10] Weibel ER. On the tricks alveolar epithelial cells play to make a good lung[J]. Am J Respir Crit Care Med, 2015, 191(5):504-513. [11] Li L, Wu W, Huang W, et al. NF-κB RNAi decreases the Bax/Bcl-2 ratio and inhibits TNF-α-induced apoptosis in human alveolar epithelial cells[J]. Inflamm Res, 2013, 62(4):387-397. [12] Kropski JA, Blackwell TS, Loyd JE. The genetic basis of idiopathic pulmonary fibrosis[J]. Eur Respir J, 2015, 45(6):1717-1727. [13] Mbeh DA, Mireles LK, Stanicki D, et al. Human alveolar epithelial cell responses to core–shell superparamagnetic iron oxide nanoparticles (SPIONs)[J]. Langmuir, 2015, 31(13):3829-3839. [14] Fujita K, Fukuda M, Fukui H, et al. Intratracheal instillation of single-wall carbon nanotubes in the rat lung induces time-dependent changes in gene expression[J]. Nanotoxicology, 2015, 9(3):290-301. [15] Kim S J, Cheresh P, Williams D, et al. Mitochondria-targeted Ogg1 and aconitase-2 prevent oxidant-induced mitochondrial DNA damage in alveolar epithelial cells[J]. J Biol Chem, 2014, 289(9):6165-6176. [16] Goncharova EA, Goncharov DA, James ML, et al. Folliculin controls lung alveolar enlargement and epithelial cell survival through E-cadherin, LKB1, and AMPK[J]. Cell Rep, 2014, 7(2):412-423. [17] Thacker S, Moran A, Lionakis M, et al. Restoration of lung surfactant protein D by IL-6 protects against secondary pneumonia following hemorrhagic shock[J].J Infect, 2014, 68(3):231-241. [18] Mao ZR, Zhang SL, Feng B. Association of IL-10 (-819T/C,-592A/C and-1082A/G) and IL-6-174G/C gene polymorphism and the risk of pneumonia-induced sepsis[J]. Biomarkers, 2017, 22(2):106-112. [19] 吴文伟, 郑世翔, 翁钦永, 等. 柚皮素缓解小鼠金黄色葡萄球菌肺炎的损伤作用及其机制[J]. 中国老年学杂志, 2015, 35(14):3849-3850.