Study on sepsis induced by liver abscess in mice due to hypervirulent Klebsiella pneumoniae
10.3760/cma.j.cn112309-20241021-00356
- VernacularTitle:高毒力肺炎克雷伯菌引发小鼠肝脓肿致脓毒症研究
- Author:
Ziwen XIE
1
;
Liming FAN
;
Weiyu JIANG
;
Keyi GONG
;
Xingdong ZHANG
;
Jiadong WANG
;
Ziyan JIANG
;
Qiang WANG
;
Jiaqi FANG
Author Information
1. 浙大城市学院医学院临床医学系，杭州 310015
- Publication Type:Journal Article
- Keywords:
Klebsiella pneumoniae;
Liver abscess;
Cytokine;
Sepsis
- From:
Chinese Journal of Microbiology and Immunology
2025;45(3):231-238
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect and preliminary mechanism of hypervirulent Klebsiella pneumoniae (hvKP) on the immune response to sepsis induced by liver abscess in mice. Methods:C57BL/6 mice were intraperitoneally injected with hvKP strain NTUH-K2044 or classical Klebsiella pneumoniae (cKP) strain HS11286 suspension to prepare the model of sepsis. The survivals rates of mice within 24 h were recorded. HE staining was used to observed the inflammatory cell infiltration in mouse liver tissues. The levels of neutrophil marker lymphocyte antigen 6G (Ly6G) in mouse liver tissues were detected by immunohistochemistry. The activity of reactive oxygen species (ROS) in mouse liver macrophages and peripheral blood monocytes was measured by ROS assay kit. The activation of p105/p50 and p65 in NF-κB signaling pathway in mouse liver macrophages and peripheral blood monocytes was detected by Western blot. The expression of IL-1β, IL-6 and TNF-α at mRNA and protein levels in mouse liver macrophages and peripheral blood monocytes were detected by qRT-PCR and ELISA, respectively. One-way analysis of variance and t test were used for statistical analysis. Results:Compared with cKP, hvKP infection could induce C57BL/6 mice to develop obvious liver abscess with massive inflammatory cell infiltration. Moreover, the level of Ly6G in liver tissues was significantly higher in hvKP-infected mice than in cKP-infected mice ( P<0.000 1), but the survival rate of hvKP-infected mice was significantly lower than that of cKP-infected mice ( P<0.000 1). hvKP significantly promoted the ROS activity ( P<0.000 1) and enhanced the phosphorylation of p105/p50 and p65 in NF-κB signaling pathway in mouse liver macrophages and peripheral blood monocytes as compared with cKP ( P<0.001). The expression of IL-1β, IL-6 and TNF-α at mRNA and protein levels in mouse liver macrophages and peripheral blood monocytes were significantly higher in hvKP-infected mice than in cKP-infected mice ( P<0.001). Conclusion:hvKP can promote the development of liver abscess and induce sepsis in mice.
