基于NLRP3/ASC/Caspase-1通路探讨SOCS-1对肺炎克雷伯菌感染的A549细胞的影响

doi:10.3870/j.issn.1672-8009.2026.04.007

摘要/Abstract

摘要： 目的基于NOD样受体家族热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)/凋亡相关斑点样蛋白(apoptosis-associated speck-like protein containing a CARD,ASC)/胱天蛋白酶-1(caspase-1)通路探讨细胞因子信号抑制物1(suppressor of cytokine signaling 1,SOCS-1)对肺炎克雷伯菌感染的A549细胞的影响。方法人Ⅱ型肺泡上皮细胞(A549细胞)被分为4个实验组:siRNA NC组、siRNA SOCS-1组、pcDNA3.1 NC组、pcDNA3.1 SOCS-1组。经肺炎克雷伯菌感染3 h后使用siRNA NC(50 nmol/L)、siRNA SOCS-1(50 nmol/L)、pcDNA3.1 NC(20 nmol/L)、pcDNA3.1 SOCS-1(20 nmol/L)处理相应的A549细胞48 h。MTT实验及BrdU染色实验分析A549细胞的增殖活性;流式细胞术分析A549细胞的凋亡率;ELISA测定各组A549细胞培养基中炎症因子水平;蛋白质印迹实验检测A549细胞中SOCS-1、NLRP3、ASC、caspase-1蛋白的表达水平。结果感染肺炎克雷伯菌能够导致A549细胞中的SOCS-1表达水平增加。与siRNA NC组比较,siRNA SOCS-1组的A549细胞增殖活性增加,凋亡率及炎症因子水平降低,NLRP3、ASC、caspase-1表达水平降低。与pcDNA3.1 NC组比较,pcDNA3.1 SOCS-1组的A549细胞增殖活性降低,凋亡率、炎症因子水平增加,NLRP3、ASC、Caspase-1表达水平增加。结论 SOCS-1能够促进肺炎克雷伯菌感染的A549细胞的凋亡及炎症因子释放水平,并抑制A549细胞增殖,这一过程与SOCS-1调控NLRP3/ASC/Caspase-1信号通路密切相关。

关键词: 细胞因子信号抑制物1, 肺炎克雷伯菌, NOD样受体蛋白3, 凋亡相关斑点样蛋白, 半胱氨酸天冬氨酸蛋白酶-1

Abstract: Objective To investigate the effects of suppressor of cytokine signaling 1(SOCS-1)on A549 cells infected with Klebsiella pneumoniae via the NOD-like receptor thermal protein domain-associated protein 3(NLRP3)/apoptosis-associated speck-like protein containing a CARD(ASC)/caspase-1 pathway. Methods Human type Ⅱ alveolar epithelial cells(A549 cells)were divided into four experimental groups:siRNA NC group,siRNA SOCS-1 group,pcDNA3.1 NC group,and pcDNA3.1 SOCS-1 group.Three hours after infection with Klebsiella pneumoniae,the corresponding A549 cells were treated with siRNA NC(50 nmol/L),siRNA SOCS-1(50 nmol/L),pcDNA3.1 NC(20 nmol/L),or pcDNA3.1 SOCS-1(20 nmol/L)for 48 h.MTT assays and BrdU staining were used to analyze the proliferative activity of A549 cells;flow cytometry was used to analyze the apoptosis rate of A549 cells;ELISA was used to determine the levels of inflammatory factors in the culture medium of A549 cells in each group;and Western blot analysis was used to detect the expression levels of SOCS-1,NLRP3,ASC,and caspase-1 proteins in A549 cells. Results Infection with Klebsiella pneumoniae led to increased SOCS-1 expression in A549 cells.Compared with the siRNA NC group,the siRNA SOCS-1 group exhibited increased A549 cell proliferation,reduced apoptosis rates and inflammatory cytokine levels,and decreased expression of NLRP3,ASC,and caspase-1.Compared with the pcDNA3.1 NC group,the pcDNA3.1 SOCS-1 group exhibited reduced A549 cell proliferation,increased apoptosis rates and levels of inflammatory factors,and elevated expression levels of NLRP3,ASC,and caspase-1. Conclusion SOCS-1 promotes apoptosis and the release of inflammatory factors in A549 cells infected with Klebsiella pneumoniae and inhibits A549 cell proliferation;this process is closely related to SOCS-1 regulation of the NLRP3/ASC/Caspase-1 signaling pathway.

Key words: suppressor of cytokine signaling 1, Klebsiella pneumoniae, NOD-like receptor protein 3, apoptosis-associated speck-like protein containing a CARD, caspase-1

中图分类号:

R563.1

娄晓, 史桂芳, 邱玙, 杜俊凤. 基于NLRP3/ASC/Caspase-1通路探讨SOCS-1对肺炎克雷伯菌感染的A549细胞的影响[J]. 医学分子生物学杂志, 2026, 23(4): 418-423.

LOU Xiao, SHI Guifang, QIU Yu, DU Junfeng. Effects of SOCS-1 on A549 Cells Infected with Klebsiella Pneumoniae via the NLRP3/ASC/Caspase-1 Pathway[J]. Journal of Medical Molecular Biology, 2026, 23(4): 418-423.

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