切换至 "中华医学电子期刊资源库"

中华实验和临床感染病杂志(电子版) ›› 2024, Vol. 18 ›› Issue (02) : 71 -74. doi: 10.3877/cma.j.issn.1674-1358.2024.02.002

综述

肺炎克雷伯菌肺炎与干扰素信号通路关系研究进展
白若靖1, 郭军1,()   
  1. 1. 102218 北京,清华大学临床医学院 清华大学附属北京清华长庚医院老年医学科
  • 收稿日期:2023-10-11 出版日期:2024-04-15
  • 通信作者: 郭军
  • 基金资助:
    清华大学精准医学科研计划(No. QT201901); 北京市卫生健康委员会高层次公共卫生技术人才建设项目培养计划(No.学科带头人-02-06)

Progress on relationship between Klebsiella pneumoniae pneumonia and interferon signaling pathway

Ruojing Bai1, Jun Guo1,()   

  1. 1. Department of Geriatric Medicine, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing 102218, China
  • Received:2023-10-11 Published:2024-04-15
  • Corresponding author: Jun Guo
引用本文:

白若靖, 郭军. 肺炎克雷伯菌肺炎与干扰素信号通路关系研究进展[J/OL]. 中华实验和临床感染病杂志(电子版), 2024, 18(02): 71-74.

Ruojing Bai, Jun Guo. Progress on relationship between Klebsiella pneumoniae pneumonia and interferon signaling pathway[J/OL]. Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Edition), 2024, 18(02): 71-74.

肺炎克雷伯菌(Kp)是一种常见的医院内及社区获得性感染的革兰阴性杆菌。考虑到Kp的耐药性和高毒力,研究其与干扰素(IFN)信号通路的相互作用对于理解其致病机制及开发新的治疗策略至关重要。本文探讨Kp肺炎与IFN信号通路间的复杂关系。IFN信号通路是固有免疫的核心部分,通过激活多种防御基因对抗病原体。Kp对IFN信号通路的激活增强了宿主免疫细胞,如自然杀伤(NK)细胞和巨噬细胞的抗菌功能。本文还揭示了IFN信号通路与炎症信号通路及自噬通路的协同作用,这对于理解Kp如何调节宿主免疫反应以逃避免疫系统的追踪具有重要意义。本文还分析了IFN信号通路在Kp肺炎治疗中的潜在应用。未来需进一步探索其疗效优化方法并降低不良反应,以应对这一日益严重的公共卫生问题。

Klebsiella pneumoniae (Kp) is a common Gram-negative bacterium that causes hospital-acquired and community-acquired infections. Considering the resistance and virulence of Kp, studying its interaction with the interferon signaling pathway is crucial for understanding its pathogenesis and developing new therapeutic strategies. This review discusses the complex relationship between Kp pneumonia and the interferon signaling pathway, which is a core part of the innate immunity that activates various defense genes against pathogens. The activation of the interferon signaling pathway by Kp enhances the antibacterial functions of host immune cells, such as natural killer (NK) cells and macrophages. This review also reveals the synergistic effects of the interferon signaling pathway with the inflammatory and autophagy pathways, which are important for understanding how Kp modulates host immune responses to evade immune surveillance. Finally, this review analyzes the potential applications of the interferon signaling pathway in the treatment of Kp pneumonia. Future research needs to further explore the optimization methods of its therapeutic effects and reduce its side effects, and to cope with this increasingly serious public health issue.

[1]
Paczosa MK, Mecsas J. Klebsiella pneumoniae: going on the offense with a strong defense[J]. Microbiol Mol Biol Rev,2016,80(3):629-661.
[2]
杭文璐, 杜永亮, 李占结, 等. 免疫功能缺陷患者碳青霉烯类耐药肺炎克雷伯菌院内感染一例[J/CD]. 中华实验和临床感染病杂志(电子版),2022,16(3):205-209.
[3]
Li S, Yu S, Peng M, et al. Clinical features and development of Sepsis in Klebsiella pneumoniae infected liver abscess patients: a retrospective analysis of 135 cases[J]. BMC Infect Dis,2021,21(1):597.
[4]
Shields RK, Zhou Y, Kanakamedala H, et al. Burden of illness in US hospitals due to carbapenem-resistant Gram-negative urinary tract infections in patients with or without bacteraemia[J]. BMC Infect Dis,2021,21(1):572.
[5]
Wu X, Shi Q, Shen S, et al. Clinical and bacterial characteristics of Klebsiella pneumoniae affecting 30-day mortality in patients with bloodstream infection[J]. Front Cell Infect Microbiol,2021,11:688989.
[6]
Luan Y, Sun Y, Duan S, et al. Pathogenic bacterial profile and drug resistance analysis of community-acquired pneumonia in older outpatients with fever[J]. J Int Med Res,2018,46(11):4596-4604.
[7]
Venkataraman R, Divatia JV, Ramakrishnan N, et al. Multicenter observational study to evaluate epidemiology and resistance patterns of common intensive care unit-infections[J]. Indian J Crit Care Med,2018,22(1):20-26.
[8]
Zhu J, Wang T, Chen L, et al. Virulence factors in hypervirulent Klebsiella pneumoniae[J]. Front Microbiol,2021,12:642484.
[9]
Coates M, Blanchard S, MacLeod AS. Innate antimicrobial immunity in the skin: a protective barrier against bacteria, viruses, and fungi[J]. PLoS Pathog,2018,14(12):e1007353.
[10]
Borden EC, Sen GC, Uze G, et al. Interferons at age 50: past, current and future impact on biomedicine[J]. Nat Rev Drug Discov,2007,6(12):975-990.
[11]
Liu T, Zhang L, Joo D, et al. NF-κB signaling in inflammation[J]. Sig Transduct Target Ther,2017,2(1):17023.
[12]
McNab F, Mayer-Barber K, Sher A, et al. Type Ⅰ interferons in infectious disease[J]. Nat Rev Immunol,2015,15(2):87-103.
[13]
Philips RL, Wang Y, Cheon H, et al. The JAK-STAT pathway at 30: much learned, much more to do[J]. Cell,2022,185(21):3857-3876.
[14]
Tam JCH, Jacques DA. Intracellular immunity: finding the enemy within--how cells recognize and respond to intracellular pathogens[J]. J Leukoc Biol,2014,96(2):233-244.
[15]
Ablasser A, Hur S. Regulation of cGAS- and RLR-mediated immunity to nucleic acids[J]. Nat Immunol,2020,21(1):17-29.
[16]
Ji L, Li T, Chen H, et al. The crucial regulatory role of type Ⅰ interferon in inflammatory diseases[J]. Nat Rev Immunol,2023,13(1):230.
[17]
Shemesh M, Lochte S, Piehler J, et al. IFNAR1 and IFNAR2 play distinct roles in initiating type Ⅰ interferon-induced JAK-STAT signaling and activating STATs[J]. Sci Signal,2021,14(710):eabe4627.
[18]
Stanifer ML, Pervolaraki K, Boulant S. Differential regulation of type Ⅰ and type Ⅲ interferon signaling[J]. Int J Mol Sci,2019,20(6):E1445.
[19]
Platanias LC. Mechanisms of type-Ⅰ- and type-Ⅱ-interferon-mediated signalling[J]. Nat Rev Immunol,2005,5(5):375-386.
[20]
Yang E, Li MMH. All about the RNA: interferon-stimulated genes that interfere with viral RNA processes[J]. Front Immunol, 2020,11:605024.
[21]
Mazewski C, Perez RE, Fish EN, et al. Type Ⅰ interferon (IFN)-regulated activation of canonical and non-canonical signaling pathways[J]. Front Immunol,2020,11:606456.
[22]
Bourdon M, Manet C, Montagutelli X. Host genetic susceptibility to viral infections: the role of type Ⅰ interferon induction[J]. Genes Immun,2020,21(6):365-379.
[23]
Zeng C, Waheed AA, Li T, et al. SERINC proteins potentiate antiviral type Ⅰ IFN production and proinflammatory signaling pathways[J]. Sci Signal,2021,14(700):eabc7611.
[24]
Ivin M, Dumigan A, de Vasconcelos FN, et al. Natural killer cell-intrinsic type Ⅰ IFN signaling controls Klebsiella pneumoniae growth during lung infection[J]. PLoS Pathog,2017,13(11):e1006696.
[25]
Doran CG, Sugisawa R, Carty M, et al. CRISPR/Cas9-mediated SARM1 knockout and epitope-tagged mice reveal that SARM1 does not regulate nuclear transcription, but is expressed in macrophages[J]. J Biol Chem,2021,297(6):101417.
[26]
Uhlen M, Oksvold P, Fagerberg L, et al. Towards a knowledge-based Human Protein Atlas[J]. Nat Biotechnol,2010,28(12):1248- 1250.
[27]
Feriotti C, Sá-Pessoa J, Calderón-González R, et al. Klebsiella pneumoniae hijacks the Toll-IL-1R protein SARM1 in a type Ⅰ IFN-dependent manner to antagonize host immunity[J]. Cell Rep,2022,40(6):111167.
[28]
Frank CG, Reguerio V, Rother M, et al. Klebsiella pneumoniae targets an EGF receptor-dependent pathway to subvert inflammation[J]. Cell Microbiol,2013,15(7):1212-1233.
[29]
Cao W, Li J, Yang K, et al. An overview of autophagy: mechanism, regulation and research progress[J]. Bull Cancer,2021,108(3):304-322.
[30]
刘会雪, 张佩佩, 安江科. 三七皂甙R1调节蛋白酪氨酸激酶2/信号转导与转录激活因子3信号通路对肺炎克雷伯菌感染的肺泡上皮细胞损伤的影响[J]. 中国热带医学,2023,23(7):754-760.
[31]
Yanai H, Taniguchi T. Fine-tuning type Ⅰ IFN signaling: a new chapter in the IFN saga[J]. Cell Res,2017,27(12):1407-1408.
[32]
Divangahi M, King IL, Pernet E. Alveolar macrophages and type I IFN in airway homeostasis and immunity[J]. Trends Immunol,2015,36(5):307-314.
[33]
Trevejo-Nuñez G, Lin B, Fan L, et al. Regnase-1 deficiency restrains Klebsiella pneumoniae infection by regulation of a type Ⅰ interferon response[J]. mBio,2021,13(1):e0379221.
[34]
López-Rodríguez JC, Hancock SJ, Li K, et al. Type Ⅰ interferons drive MAIT cell functions against bacterial pneumonia[J]. J Exp Med,2023,220(10):e20230037.
[1] 樊恒, 孙敏, 朱建华. 红景天苷通过抑制PI3K/AKT/mTOR信号通路对大鼠脓毒症急性肾损伤的保护作用[J/OL]. 中华危重症医学杂志(电子版), 2024, 17(03): 188-195.
[2] 唐丹, 姚晓曦, 杨博文, 薛绍龙, 李梦瑶, 韦柳杏, 郄明蓉. 双肾上腺皮质激素样激酶1对子宫内膜样腺癌患者临床特征的影响[J/OL]. 中华妇幼临床医学杂志(电子版), 2024, 20(05): 582-590.
[3] 郑宝英, 黄小兰, 贾楠, 朱春梅. 儿童难治性肺炎支原体肺炎早期预警指标[J/OL]. 中华实验和临床感染病杂志(电子版), 2024, 18(04): 215-221.
[4] 李亚萍, 张萌, 李博驹, 刘晨瑞, 苟国娥, 李嘉昕, 张玉凤, 席淼, 邓慧玲. 干扰素诱导蛋白16-干扰素基因刺激因子通路在柯萨奇病毒A6型感染手足口病患儿的表达及其临床意义[J/OL]. 中华实验和临床感染病杂志(电子版), 2024, 18(03): 135-141.
[5] 狄静怿, 陈禹江, 陈欣欣, 陈文霞. 基质细胞衍生因子1通过PI3K/AKT1信号通路对巨噬细胞极化的影响[J/OL]. 中华口腔医学研究杂志(电子版), 2024, 18(02): 89-95.
[6] 李智, 冯芸. NF-κB 与MAPK 信号通路及其潜在治疗靶点在急性呼吸窘迫综合征中的研究进展[J/OL]. 中华肺部疾病杂志(电子版), 2024, 17(05): 840-843.
[7] 陈冬丽, 邓迎丽, 毕婧. α-干扰素治疗急性呼吸道病毒感染对Th1/Th2平衡及肺功能的影响[J/OL]. 中华肺部疾病杂志(电子版), 2024, 17(04): 590-594.
[8] 张敏, 朱建华, 缪雅芳, 郭锦荣. 菝葜皂苷元对肝癌HepG2细胞抑制作用的机制研究[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(06): 328-335.
[9] 季加翠, 孙春斌, 罗恩丽. 姜黄素通过调节NF-κB/NLRP3通路减轻LPS诱导小胶质细胞神经炎症损伤[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(04): 193-203.
[10] 李博, 马秀岩, 孙杰. lncRNA TINCR对滋养层HTR-8/SVneo细胞生物学行为的影响及其机制[J/OL]. 中华细胞与干细胞杂志(电子版), 2024, 14(03): 167-172.
[11] 阿卜杜萨拉木·图尔荪麦麦提, 吐尔洪江·吐逊, 温浩. 肝脏缺血-再灌注损伤与cGAS-STING信号通路[J/OL]. 中华肝脏外科手术学电子杂志, 2024, 13(03): 394-397.
[12] 胡静, 杨秀锦, 侯志云. HBV感染患者外周血ISGs表达水平变化及其与干扰素治疗疗效的关系[J/OL]. 中华消化病与影像杂志(电子版), 2024, 14(04): 343-347.
[13] 靳英, 付小霞, 陈美茹, 袁璐, 郝力瑶. CD147调控MAPK信号通路对结肠癌细胞增殖和凋亡的影响及机制研究[J/OL]. 中华临床医师杂志(电子版), 2024, 18(05): 474-480.
[14] 孙琳, 韩萍萍, 张碧琳, 张军霞. 血清WISP1水平与2型糖尿病患者血尿酸升高的相关性[J/OL]. 中华临床医师杂志(电子版), 2024, 18(02): 178-182.
[15] 陈秋怡, 林熙, 刘珍银. 淋巴管畸形分子机制的研究进展[J/OL]. 中华介入放射学电子杂志, 2024, 12(04): 374-379.
阅读次数
全文


摘要