Advances in research on Nod-like receptor protein 3 inflammasome in parasitic diseases

doi:10.12140/j.issn.1000-7423.2020.03.021

Abstract

Abstract:

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.

Key words: Parasitic disease, Nod-like receptor protein 3 inflammasome, Inflammation, Immune response

CLC Number:

CHEN Cai-song, ZHANG Yao-gang, WANG Zhi-xin, FAN Hai-ning. Advances in research on Nod-like receptor protein 3 inflammasome in parasitic diseases[J]. CHINESE JOURNAL OF PARASITOLOGY AND PARASITIC DISEASES, 2020, 38(3): 390-394.

References 43

[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. doi: 10.1016/s1097-2765(02)00599-3 pmid: 12191486
[2]	Man SM, Kanneganti TD. Gasdermin D: the long-awaited executioner of pyroptosis[J]. Cell Res, 2015,25(11):1183-1184. pmid: 26482951
[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. doi: 10.1038/ng756 pmid: 11687797
[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. doi: 10.4049/jimmunol.0901363 pmid: 19570822
[5]	Zhou RB, Yazdi AS, Menu P, et al. A role for mitochondria in NLRP3 inflammasome activation[J]. Nature, 2011,469(7329):221-225. doi: 10.1038/nature09663 pmid: 21124315
[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. doi: 10.1073/pnas.1117765109 pmid: 22733741
[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. doi: 10.1038/nature08938 pmid: 20428172
[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. doi: 10.1038/ni.1631 pmid: 18604214
[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. pmid: 30153825
[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. doi: 10.1038/ni.3772 pmid: 28722711
[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. pmid: 2050326
[12]	Iyer SS, He Q, Janczy JR, et al. Mitochondrial cardiolipin is required for NLRP3 inflammasome activation[J]. Immunity, 2013,39(2):311-323. doi: 10.1016/j.immuni.2013.08.001 pmid: 23954133
[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. doi: 10.1038/nature16959 pmid: 26814970
[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. doi: 10.1038/ni.3333 pmid: 26642356
[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. doi: 10.1016/j.molcel.2012.11.009 pmid: 23246432
[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. doi: 10.1038/nature03342 pmid: 15759000
[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. pmid: 6166564
[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. doi: 10.1016/j.meegid.2016.02.038 pmid: 26946405
[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. doi: 10.1186/1471-2164-11-63 pmid: 20102605
[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. doi: 10.1371/journal.ppat.1004887 pmid: 25955828
[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. doi: 10.1038/s41385-018-0101-9 pmid: 30361535
[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. doi: 10.1007/s10900-019-00684-z pmid: 31222620
[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. doi: 10.1371/journal.pone.0111539 pmid: 25372293
[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. doi: 10.4049/jimmunol.173.9.5688 pmid: 15494520
[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. doi: 10.4049/jimmunol.177.6.3515 pmid: 16951309
[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. doi: 10.4049/jimmunol.1003911 pmid: 21753151
[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. pmid: 11818448
[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. doi: 10.1016/j.bbadis.2017.01.006 pmid: 28087471
[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. pmid: 9488415
[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. doi: 10.4049/jimmunol.0902254 pmid: 20042586
[33]	Gonçalves 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. doi: 10.1371/journal.pntd.0002469 pmid: 24098823
[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. doi: 10.1016/j.chom.2017.12.002 pmid: 29290574
[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. doi: 10.1038/nm.3221 pmid: 23749230
[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. doi: 10.1371/journal.pntd.0003868 pmid: 26114647
[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). doi: 10.1111/pim.12434 pmid: 28380250
[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. doi: 10.1371/journal.pntd.0000412 pmid: 19707588
[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. doi: 10.18632/oncotarget.10044 pmid: 27322427
[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)
	( 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.)