收稿日期: 2019-08-26
网络出版日期: 2020-07-07
基金资助
国家重点研发计划“精准医学研究重点”专项(2017YFC0909900);青海省科技厅项目(2019-SF-131);青海省卫计委指导性重点项目(2016-wjzd-04)
Advances in research on Nod-like receptor protein 3 inflammasome in parasitic diseases
Received date: 2019-08-26
Online published: 2020-07-07
Supported by
National Major Research and Development Project of Precision Medicine Research(2017YFC0909900);Qinghai Province Science and Technology Department Programme(2019-SF-131);Qinghai Province Health and Family Planning Commission Programme(2016-wjzd-04)
炎症小体作为固有免疫系统的感受器,活化后可以参与抵抗病原生物体的应激反应。本文总结归纳了Nod样受体蛋白3（NLRP3）炎症小体的基本结构、功能及其在疟疾、溶组织内阿米巴病、克氏锥虫病、利什曼原虫病、血吸虫病、阴道毛滴虫病中的相关研究,旨在分析NLRP3炎症小体在寄生虫病中的作用及机制,为干预与治疗手段优化提供思路。
关键词： 寄生虫病; Nod样受体蛋白3炎症小体; 炎症; 免疫反应
陈蔡松 , 张耀刚 , 王志鑫 , 樊海宁 . Nod样受体蛋白3炎症小体在寄生虫病中的研究进展[J]. 中国寄生虫学与寄生虫病杂志, 2020 , 38(3) : 390 -394 . DOI: 10.12140/j.issn.1000-7423.2020.03.021
Inflammatory corpuscles are receptors of the innate immune system and participate in the stress responses against pathogenic organisms after activated. This review summarizes the basic structure and functions of Nod-like receptor protein 3 (NLRP3) inflammasome as well as the related researches on malaria, amoebic disease, trypanosomiasis, leishmaniasis, schistosomiasis, and vaginal trichomoniasis, aiming to analyze the role and mechanism of NLRP3 inflammasome in parasitic diseases and provide ideas for better interventions and treatment.
| [1] | Martinon F, Burns K, Tschopp J. The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of pro-IL-beta[J]. Mol Cell, 2002,10(2):417-426. |
| [2] | Man SM, Kanneganti TD. Gasdermin D: the long-awaited executioner of pyroptosis[J]. Cell Res, 2015,25(11):1183-1184. |
| [3] | Hoffman HM, Mueller JL, Broide DH, et al. Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndrome[J]. Nat Genet, 2001,29(3):301-305. |
| [4] | Bauernfeind FG, Horvath G, Stutz A, et al. Cutting edge: NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression[J]. J Immunol, 2009,183(2):787-791. |
| [5] | Zhou RB, Yazdi AS, Menu P, et al. A role for mitochondria in NLRP3 inflammasome activation[J]. Nature, 2011,469(7329):221-225. |
| [6] | Murakami T, Ockinger J, Yu J, et al. Critical role for calcium mobilization in activation of the NLRP3 inflammasome[J]. Proc Natl Acad Sci USA, 2012,109:11282-1128. |
| [7] | Duewell P, Kono H, Rayner KJ, et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals[J]. Nature, 2010,464(7293):1357-1361. |
| [8] | Hornung V, Bauernfeind F, Halle A, et al. Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization[J]. Nat Immunol, 2008,9(8):847-856. |
| [9] | Gong Z, Pan JR, Shen QY, et al. Mitochondrial dysfunction induces NLRP3 inflammasome activation during cerebral ischemia/reperfusion injury[J]. J Neuroinflammation, 2018,15(1):242. |
| [10] | Afonina IS, Zhong ZY, Karin M, et al. Limiting inflammation-the negative regulation of NF-κB and the NLRP3 inflammasome[J]. Nat Immunol, 2017,18(8):861-869. |
| [11] | Wree A, McGeough MD, Inzaugarat ME, et al. The NLRP3 inflammasome, a caspase-1 activation platform, plays a key role in the modulation of liver inflammation and fibrosis[J]. Hepatology, 2017,13. |
| [12] | Iyer SS, He Q, Janczy JR, et al. Mitochondrial cardiolipin is required for NLRP3 inflammasome activation[J]. Immunity, 2013,39(2):311-323. |
| [13] | He Y, Zeng MY, Yang DH, et al. NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux[J]. Nature, 2016,530(7590):354-357. |
| [14] | Shi HX, Wang Y, Li XH, et al. NLRP3 activation and mitosis are mutually exclusive events coordinated by NEK7, a new inflammasome component[J]. Nat Immunol, 2016,17(3):250-258. |
| [15] | Py BF, Kim MS, Vakifahmetoglu-Norberg H, et al. Deubiquitination of NLRP3 by BRCC3 critically regulates inflammasome activity[J]. Mol Cell, 2013,49(2):331-338. |
| [16] | Snow RW, Guerra CA, Noor AM, et al. The global distribution of clinical episodes of Plasmodium falciparum malaria[J]. Nature, 2005,434(7030):214-217. |
| [17] | Shio MT, Eisenbarth SC, Savaria M, et al. Correction: malarial hemozoin activates the NLRP3 inflammasome through lyn and syk kinases[J]. PLoS Pathog, 2009,5(9):1000559. |
| [18] | Griffith JW, Sun T, McIntosh MT, et al. Pure hemozoin is inflammatory in vivo and activates the NALP3 inflammasome via release of uric acid[J]. Immunol, 2009,183(8):5208-5220. |
| [19] | Clark IA, Virelizier JL, Carswell EA, et al. Possible importance of macrophage-derived mediators in acute malaria[J]. Infect Immun, 1981,32(3):1058-1066. |
| [20] | Santos MLS, Reis EC, Bricher PN, et al. Contribution of inflammasome genetics in Plasmodium vivax malaria[J]. Infect Genet Evol, 2016,40:162-166. |
| [21] | Biller L, Davis PH, Tillack M, et al. Differences in the transcriptome signatures of two genetically related Entamoeba histolytica cell lines derived from the same isolate with different pathogenic properties[J]. BMC Genomics, 2010,11:63. |
| [22] | Mortimer L, Moreau F, Cornick S, et al. The NLRP3 inflammasome is a pathogen sensor for invasive Entamoeba histolytica via activation of α5β1 integrin at the macrophage-amebae intercellular junction[J]. PLoS Pathog, 2015,11(5):e1004887. |
| [23] | Quach J, Moreau F, Sandall C, et al. Entamoeba histolytica-induced IL-1β secretion is dependent on caspase-4 and gasdermin D[J]. Mucosal Immunol, 2019,12(2):323-339. |
| [24] | Gómez IPJ, Peremiquel-Trillas P, Claveria GI, et al. A community-based intervention for the detection of chagas disease in Barcelona, Spain[J]. J Community Health, 2019,44(4):704-711. |
| [25] | Dey N, Sinha M, Gupta S, et al. Caspase-1/ASC inflammasome-mediated activation of IL-1β-ROS-NF-κB pathway for control of Trypanosoma cruzi replication and survival is dispensable in NLRP3-/-macrophages[J]. PLoS One, 2014,9(11):e111539. |
| [26] | Oliveira AC, Peixoto JR, de Arruda LB, et al. Expression of functional TLR4 confers proinflammatory responsiveness to Trypanosoma cruzi glycoinositolphospholipids and higher resistance to infection with T. cruzi[J]. J Immunol, 2004,173(9):5688-5696. |
| [27] | Bafica A, Santiago HC, Goldszmid R, et al. Cutting edge: TLR9 and TLR2 signaling together account for MyD88-dependent control of parasitemia in Trypanosoma cruzi infection[J]. J Immunol, 2006,177(6):3515-3519. |
| [28] | Caetano BC, Carmo BB, Melo MB, et al. Requirement of UNC93B1 reveals a critical role for TLR7 in host resistance to primary infection with Trypanosoma cruzi[J]. J Immunol, 2011,187(4):1903-1911. |
| [29] | Bastos KR, Alvarez JM, Marinho CR, et al. Macrophages from IL-12p40-deficient mice have a bias toward the M2 activation profile[J]. J Leukoc Biol, 2002,71(2):271-278. |
| [30] | Sanmarco LM, Ponce NE, Visconti LM, et al. IL-6 promotes M2 macrophage polarization by modulating purinergic signaling and regulates the lethal release of nitric oxide during Trypanosoma cruzi infection[J]. Biochim Biophys Acta Mol Basis Dis, 2017,1863(4):857-869. |
| [31] | Holscher C, Kohler G, Muller U, et al. Defective nitric oxide effector functions lead to extreme susceptibility of Trypanosoma cruzi-infected mice deficient in gamma interferon receptor or inducible nitric oxide synthase[J]. Infect Immun, 1998,66(3):1208-1215. |
| [32] | Silva GK, Gutierrez FR, Guedes PM, et al. Cutting edge: nucleotide-binding oligomerization domain 1-dependent responses account for murine resistance against Trypanosoma cruzi infection[J]. J Immunol, 2010,184(3):1148-1152. |
| [33] | Gon?alves VM, Matteucci KC, Buzzo CL, et al. NLRP3 controls Trypanosoma cruzi infection through a caspase-1-dependent IL-1R-independent NO production[J]. PLoS Negl Trop Dis, 2013,7(10):e2469. |
| [34] | Dey R, Joshi AB, Oliveira F, et al. Gut microbes egested during bites of infected sand flies augment severity of leishmaniasis via inflammasome-derived IL-1β[J]. Cell Host Microbe, 2018,23(1):134-143. |
| [35] | Lima-Junior DS, Costa DL, Carregaro V, et al. Inflammasome-derived IL-1β production induces nitric oxide-mediated resistance to Leishmania[J]. Nat Med, 2013,19(7):909-915. |
| [36] | Shio MT, Christian JG, Jung JY, et al. PKC/ROS-mediated NLRP3 inflammasome activation is attenuated by Leishmania zinc-metalloprotease during infection[J]. PLoS Negl Trop Dis, 2015,9(6):e0003868. |
| [37] | Moreira RB, Pirmez C, de Oliveira-Neto MP, et al. AIM2 inflammasome is associated with disease severity in tegumentary leishmaniasis caused by Leishmania(V.) braziliensis[J]. Parasite Immunol, 2017,39(7). |
| [38] | Hotez PJ, Kamath A. Neglected tropical diseases in sub-Saharan Africa: review of their prevalence, distribution, and disease burden[J]. PLoS Negl Trop Dis, 2009,3(8):e412. |
| [39] | Elmorshedy H, Bergquist R, El-Ela NE, et al. Can human schistosomiasis mansoni control be sustained in high-risk transmission foci in Egypt?[J]. Parasit Vectors, 2015,8:372. |
| [40] | Ritter M, Gross O, Kays S, et al. Schistosoma mansoni triggers Dectin-2, which activates the NLRP3 inflammasome and alters adaptive immune responses[J]. Proc Natl Acad Sci USA, 2010,107(47):20459-20464. |
| [41] | Meng N, Xia M, Lu YQ, et al. Activation of NLRP3 inflammasomes in mouse hepatic stellate cells during Schistosoma infection[J]. Oncotarget, 2016,7(26):39316-39331. |
| [42] | Gu NY, Kim JH, Han IH, et al. Trichomonas vaginalis induces IL-1β production in a human prostate epithelial cell line by activating the NLRP3 inflammasome via reactive oxygen species and potassium Ion efflux[J]. Prostate, 2016,76(10):885-896. |
| [43] | Wen ZC, Ji XF, Lin GY, et al. NLRP3 inflammasome activation in liver is associated with the extent of hepatic fibrosis in mice infected with Schistosoma japonicum[J]. Chin J Parasitol Parasit Dis, 2017, 35(4): 3-322-326. (in Chinese) |
| [43] | ( 温镇成, 季小芳, 林桂莹, 等. 肝组织中NLRP3炎症小体活化与日本血吸虫感染小鼠肝纤维化程度的相关性[J]. 中国寄生虫学与寄生虫病杂志, 2017, 35(4): 3-322-326.) |
/
| 〈 |
|
〉 |