miR-223 inhibits pulmonary lesions of rats with pulmonary tuberculosis

doi:10.16352/j.issn.1001-6325.2022.08.1225

Abstract

Abstract: Objective To explore the effect of miR-223 on pulmonary lesions and IFN-γ in rats with pulmonary tuberculosis(PT) mechanism of protein expression. Methods Rats were divided into normal group (NC group), pulmonary tuberculosis rat model group (PT group) and pulmonary tuberculosis rat model transfected with miR-223 mimics group (miR-223 group) with 10 in each group. T cells in peripheral blood was quantified by flow cytometry, IFN-γ in serum was detected by ELISA and IL-18 levels, and the number of Mycobacterium tuberculosis colonies was counted; the pathological changes of lung tissue were micros copied by HE staining; IFN-γ in lung tissue was detected by immunohistochemistry method; RT-qPCR was used to detect miR-223 mRNA and IFN-γ in lung tissue MRNA expression. Results In PT group, the peripheral blood T cell subsets were disordered, the level of CD3⁺,CD4⁺% significantly decreased, and CD8⁺% was increased (P＜0.05); CD3⁺ and CD4⁺ percentage in miR-223 group were higher than those in PT group, while the percentage of CD8⁺ was lower(P＜0.05). Serum IFN-γ and IL-18 in PT group increased(P＜0.05); the number of Mycobacterium tuberculosis colonies in PT group was more than that in NC group (P＜0.05); the colony number of Mycobacterium tuberculosis in miR-223 group was significantly less than that in PT group (P＜0.05). Total IFN-γ level in PT group was higher than that in NC group(P＜0.05) but was significantly inhibited in miR-223 group(P＜0.05). Conclusions miR-223 can inhibit the pulmonary inflammatory response caused by Mycobacterium tuberculosis, and miR-223 showed an effect of anti-tuberculosis bacteria and may regulate host immunity, so and can effectively inhibit the expression of IFN-γ in lung tissue and thus alleviates severity of tuberculosis.

Key words: miR-223, pulmonary tuberculosis, pulmonary lesions, IFN-γ protein

CLC Number:

R521

TONG Xiao-wei, XIAO Han. miR-223 inhibits pulmonary lesions of rats with pulmonary tuberculosis[J]. Basic & Clinical Medicine, 2022, 42(8): 1225-1229.

References 15

[1]	Kweza PF, Van SC, Abraham N, et al. Estimating the magnitude of pulmonary tuberculosis patients missed by primary health care clinics in South Africa[J]. Int J Tuberc Lung Dis, 2018, 22:264-272.
[2]	Castro-Garza J. Mycobacterium tuberculosis promotes genomic instability in macrophages[J]. Mem Inst Oswaldo Cruz, 2018,113:161-166.
[3]	杜伟勤, 任建斌. γ干扰素,骨桥蛋白,白细胞介素-18在肺结核患者血清与痰液上清液中的表达与临床意义[J]. 中国当代医药, 2010, 27:12-15.
[4]	张文玲, 周学东, 郝玉庆,等. microRNA:一种潜在新型诊断结核病的生物标志物[J]. 四川大学学报:自然科学版, 2015, 52:1399-1403.
[5]	魏文燕, 陈建英. 非编码RNA调控巨噬细胞极化的研究进展[J]. 山东医药,2018, 58:90-94.
[6]	虞秀锋, 王启源, 姬文兰,等. MiR-506-3p/SOCS-3促进BCG感染巨噬细胞引发的炎症应答反应[J]. 中国人兽共患病学报, 2020, 36:297-302.
[7]	Coler RN, Day TA, Ruth E, et al. The TLR-4 agonist adjuvant, GLA-SE, improves magnitude and quality of immune responses elicited by the ID93 tuberculosis vaccine:first-in-human trial[J]. NPJ Vaccines, 2018,3:34.doi:10.1038/s41541-018-0057-5.
[8]	方志雄, 徐磊, 张海明,等. 肺结核患者血液和痰液中特异性CD4+T淋巴细胞CD27表达水平及其诊断新发肺结核的价值[J]. 广西医学, 2019, 41:3109-3113.
[9]	邓清, 张铁泉, 乐问津,等. 长链非编码RNA DRAIC调控miR-223对胃癌细胞迁移和侵袭的影响[J]. 西部医学, 2018, 30:1753-1757.
[10]	何畏, 陈晴, 黄涛, 等. 肺结核及肺外结核患者外周血T淋巴细胞亚群的变化及其临床意义[J]. 中国防痨杂志, 2019,41:1090-1095.
[11]	蔡灵芝, 何丽波, 林宇航,等. 活动性结核患者结核分枝杆菌抗原特异性多能T淋巴细胞细胞因子的分泌特征[J]. 中华医院感染学杂志, 2019, 29:179-183.
[12]	田杰, 郭淑湘. 活动性肺结核患者痰液及血清中骨桥蛋白,白细胞介素-18和干扰素-γ的检测及意义[J]. 标记免疫分析与临床, 2015, 22:540.
[13]	Roffel MP, Bracke KR, Heijink IH, et al. miR-223:A key regulator in the innate immune response in asthma and COPD[J]. Front Med, 2010, 1:196.doi:10.3389/fmed.2020.00196.
[14]	洪爱玲,朱海燕,何贵清,等.miRNA-223靶向FoxO3抑制肺结核大鼠巨噬细胞凋亡研究[J].浙江医学,2019,41:1610-1613.
[15]	Liu Y,Wang R,Jiang J,et al.miR-223 is upregulated in monocytes from patients with tuberculosis and regulates function of monocyte-derived macrophages[J].Mol Immunol,2015,67:475-481.