细胞焦亡在人体寄生虫病中的研究进展

doi:10.12140/j.issn.1000-7423.2022.06.014

中国寄生虫学与寄生虫病杂志 ›› 2022, Vol. 40 ›› Issue (6): 780-785.doi: 10.12140/j.issn.1000-7423.2022.06.014

细胞焦亡在人体寄生虫病中的研究进展

乜茹¹^,²^,³(), 李文登¹^,², 冶赓博¹^,²^,³, 尹凤娇¹^,²^,³, 庞明泉¹^,², 王志鑫¹^,², 樊海宁¹^,²^,^*()

1.青海大学附属医院肝胆胰外科，西宁 810001
2.青海省包虫病研究重点实验室，西宁810001
3.青海大学研究生院，西宁 810001

收稿日期:2022-05-29 修回日期:2022-08-29 出版日期:2022-12-30 发布日期:2022-12-26
通讯作者: 樊海宁
作者简介:乜茹(1987-)，女，硕士研究生，从事棘球蚴免疫研究工作。E-mail：zzzsruru@163.com
基金资助:
青海省科技厅重点实验室项目(2020-ZJ-Y01);青海大学附属医院中青年科研基金一般项目(ASRF-2019-YB-04)

Research progress on the role of pyroptosis in human parasitic diseases

NIE Ru¹^,²^,³(), LI Wen-deng¹^,², YE Geng-bo¹^,²^,³, YIN Feng-jiao¹^,²^,³, PANG Ming-quan¹^,², WANG Zhi-xin¹^,², FAN Hai-ning¹^,²^,^*()

1. Department of Hepatopancreatobiliary Surgery, the Affiliated Hospital of Qinghai University, Xining 810001, China
2. Qinghai Province Key Laboratory of Hydatid Disease Research, Xining 810001, China
3. Graduate School of Qinghai University, Xining 810001, China

Received:2022-05-29 Revised:2022-08-29 Online:2022-12-30 Published:2022-12-26
Contact: FAN Hai-ning
Supported by:
Key Laboratory Project of Qinghai Provincial Science and Technology Department(2020-ZJ-Y01);Qinghai University Affiliated Hospital, General Project of Young and Middle-aged Research Fund(ASRF-2019-YB-04)

摘要/Abstract

摘要：

细胞焦亡是近年发现的一种依赖半胱氨酸天冬氨酸蛋白酶（caspase）的新型细胞死亡方式，活化后的caspase以剪切消皮素（GSDM）蛋白家族为途径，使细胞膜发生破裂，同时释放炎性细胞因子及其内容物，最终导致细胞死亡，其发生、形态学特征及调控机制与凋亡、坏死、自噬、铁死亡等细胞死亡方式有明显不同。细胞焦亡信号通路可分为经典途径、非经典途径和其他途径。目前大量研究证实，细胞焦亡参与寄生虫病的发展历程。本文就细胞焦亡的定义、不同途径机制及其在多种人体寄生虫病中发挥的作用作一综述，以期为开拓细胞焦亡与寄生虫疾病之间的作用提供依据。

关键词: 细胞焦亡, 消皮素, 半胱氨酸天冬氨酸蛋白酶, Nod样受体蛋白3, 人体寄生虫病

Abstract:

Pyroptosis is a new type of death mode found in recent years, which depends on caspase. Activated caspase breaks the cell membrane by cutting gasdermin protein, and at the same time, it releases pro-inflammatory cytokines and their contents, eventually leading to cell death. Its occurrence, morphological characteristics and regulatory mechanism are different from cell death modes such as apoptosis, necrosis, autophagy and iron death. Pyroptosis signal pathways include classical pathway, non-classical pathway and other pathways. At present, many studies have confirmed that pyroptosis is involved in the development of parasitic diseases. This article reviews the definition of pyroptosis, different pathways and mechanisms, and their roles in various Human parasitic diseases, hoping to provide a basis for developing the research between pyroptosis and parasitic diseases.

Key words: Pyroptosis, Gasdermin protein, Caspase, Nod-like receptor protein 3, Human parasitic disease

中图分类号:

乜茹, 李文登, 冶赓博, 尹凤娇, 庞明泉, 王志鑫, 樊海宁. 细胞焦亡在人体寄生虫病中的研究进展[J]. 中国寄生虫学与寄生虫病杂志, 2022, 40(6): 780-785.

NIE Ru, LI Wen-deng, YE Geng-bo, YIN Feng-jiao, PANG Ming-quan, WANG Zhi-xin, FAN Hai-ning. Research progress on the role of pyroptosis in human parasitic diseases[J]. Chinese Journal of Parasitology and Parasitic Diseases, 2022, 40(6): 780-785.

参考文献 65

[1]	Kaste SC, Pratt CB, Cain AM, et al. Metastases detected at the time of diagnosis of primary pediatric extremity osteosarcoma at diagnosis: imaging features[J]. Cancer, 1999, 86(8): 1602-1608. doi: 10.1002/(sici)1097-0142(19991015)86:8<1602::aid-cncr31>3.0.co;2-r pmid: 10526292
[2]	Wu JL, Lin S, Wan B, et al. Pyroptosis in liver disease: new insights into disease mechanisms[J]. Aging Dis, 2019, 10(5): 1094-1108 doi: 10.14336/AD.2019.0116
[3]	Shi JJ, Zhao Y, Wang YP, et al. Inflammatory caspases are innate immune receptors for intracellular LPS[J]. Nature, 2014, 514(7521): 187-192. doi: 10.1038/nature13683
[4]	Minton K. Pyroptosis heats tumour immunity[J]. Nat Rev Immunol, 2020, 20(5): 274-275. doi: 10.1038/s41577-020-0297-2 pmid: 32203327
[5]	Cui QT, Wang JH, Liu XC, et al. Knockout of PTEN improves cardiac function and inhibits NLRP3-mediated cardiomyocyte pyroptosis in rats with myocardial ischemia-reperfusion[J]. Chin J Cell Mol Immunol, 2020, 36(3): 205-211. (in Chinese)
	(崔勤涛, 王俊华, 刘晓晨, 等. 敲除PTEN改善心肌缺血再灌注大鼠心脏功能并抑制NLRP3介导的心肌细胞焦亡[J]. 细胞与分子免疫学杂志, 2020, 36(3): 205-211.)
[6]	Doitsh G, Galloway NLK, Geng X, et al. Cell death by pyroptosis drives CD4 T-cell depletion in HIV-1 infection[J]. Nature, 2014, 505(7484): 509-514. doi: 10.1038/nature12940
[7]	Kong DL, Kong FY, Liu XY, et al. Soluble egg antigen of Schistosoma japonicum induces pyroptosis in hepatic stellate cells by modulating ROS production[J]. Parasit Vectors, 2019, 12(1): 475. doi: 10.1186/s13071-019-3729-8 pmid: 31610797
[8]	Saha G, Khamar B, Kumar M, et al. Unraveling the role of BLIMP-1 induction during Leishmania donovani infection as a novel escape mechanism[C]. Beijing:17th International Congress of Immunology, 2019: 191-192. (in Chinese)
	(Saha G, Khamar B, Kumar M, et al. Unraveling the role of BLIMP-1 induction during Leishmania donovani infection as a novel escape mechanism[C]. 北京: 第十七届国际免疫学大会, 2019: 191-192.)
[9]	Chen Y, Smith MR, Thirumalai K, et al. A bacterial invasin induces macrophage apoptosis by binding directly to ICE[J]. EMBO J, 1996, 15(15): 3853-3860. pmid: 8670890
[10]	Cookson BT, Brennan MA. Pro-inflammatory programmed cell death[J]. Trends Microbiol, 2001, 9(3): 113-114. doi: 10.1016/s0966-842x(00)01936-3 pmid: 11303500
[11]	Qiu SQ, Liu J, Xing FY. ‘Hints’ in the killer protein gasdermin D: unveiling the secrets of gasdermins driving cell death[J]. Cell Death Differ, 2017, 24(4): 588-596. doi: 10.1038/cdd.2017.24
[12]	Kayagaki N, Warming S, Lamkanfi M, et al. Non-canonical inflammasome activation targets caspase-11[J]. Nature, 2011, 479(7371): 117-121. doi: 10.1038/nature10558
[13]	Shi JJ, Gao WQ, Shao F. Pyroptosis: gasdermin-mediated programmed necrotic cell death[J]. Trends Biochem Sci, 2017, 42(4): 245-254. doi: S0968-0004(16)30182-7 pmid: 27932073
[14]	Ruan JW, Wang SJ, Wang JB. Mechanism and regulation of pyroptosis-mediated in cancer cell death[J]. Chem Biol Interact, 2020, 323: 109052.
[15]	Shi JJ, Zhao Y, Wang K, et al. Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death[J]. Nature, 2015, 526(7575): 660-665. doi: 10.1038/nature15514
[16]	Sborgi L, Rühl S, Mulvihill E, et al. GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death[J]. EMBO J, 2016, 35(16): 1766-1778. doi: 10.15252/embj.201694696 pmid: 27418190
[17]	Zhou ZW, He HB, Wang K, et al. Granzyme A from cytotoxic lymphocytes cleaves GSDMB to trigger pyroptosis in target cells[J]. Science, 2020, 368(6494): eaaz7548. doi: 10.1126/science.aaz7548
[18]	Zhang ZB, Zhang Y, Xia SY, et al. Gasdermin E suppresses tumour growth by activating anti-tumour immunity[J]. Nature, 2020, 579(7799): 415-420. doi: 10.1038/s41586-020-2071-9
[19]	Galluzzi L, Vitale I, Aaronson SA, et al. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018[J]. Cell Death Differ, 2018, 25(3): 486-541. doi: 10.1038/s41418-017-0012-4 pmid: 29362479
[20]	Ivanov K, Garanina E, Rizvanov A, et al. Inflammasomes as targets for adjuvants[J]. Pathogens, 2020, 9(4): 252. doi: 10.3390/pathogens9040252
[21]	Chen CS, Zhang YG, Wang ZX, et al. Advances in research on Nod-like receptor protein 3 inflammasome in parasitic diseases[J]. Chin J Parasitol Parasit Dis, 2020, 38(3): 390-394. (in Chinese)
	(陈蔡松, 张耀刚, 王志鑫, 等. 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.)
[22]	Sborgi L, Rühl S, Mulvihill E, et al. GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death[J]. EMBO J, 2016, 35(16): 1766-1778. doi: 10.15252/embj.201694696 pmid: 27418190
[23]	Gong CY, Cheng P, Zhang HH. Roles of NLRP3 inflammasome in intervertebral disc degeneration[J]. Osteoarthritis Cartilage, 2021, 29(6): 793-801. doi: 10.1016/j.joca.2021.02.204
[24]	Jorgensen I, Miao EA. Pyroptotic cell death defends against intracellular pathogens[J]. Immunol Rev, 2015, 265(1): 130-142. doi: 10.1111/imr.12287 pmid: 25879289
[25]	Yang JL, Zhao Y, Shao F. Non-canonical activation of inflammatory caspases by cytosolic LPS in innate immunity[J]. Curr Opin Immunol, 2015, 32: 78-83. doi: 10.1016/j.coi.2015.01.007 pmid: 25621708
[26]	Meunier E, Dick MS, Dreier RF, et al. Caspase-11 activation requires lysis of pathogen-containing vacuoles by IFN-induced GTPases[J]. Nature, 2014, 509(7500): 366-370. doi: 10.1038/nature13157
[27]	Chen KW, Demarco B, Broz P. Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation[J]. Eur J Immunol, 2020, 50(2): 170-177. doi: 10.1002/eji.201948254 pmid: 31411729
[28]	Sarhan J, Liu BC, Muendlein HI, et al. Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis during Yersinia infection[J]. Proc Natl Acad Sci USA, 2018, 115(46): E10888-E10897.
[29]	Zhang ZB, Zhang Y, Xia SY, et al. Gasdermin E suppresses tumour growth by activating anti-tumour immunity[J]. Nature, 2020, 579(7799): 415-420. doi: 10.1038/s41586-020-2071-9
[30]	Kambara H, Liu F, Zhang XY, et al. Gasdermin D exerts anti-inflammatory effects by promoting neutrophil death[J]. Cell Rep, 2018, 22(11): 2924-2936. doi: S2211-1247(18)30261-4 pmid: 29539421
[31]	Kayagaki N, Kornfeld OS, Lee BL, et al. NINJ1 mediates plasma membrane rupture during lytic cell death[J]. Nature, 2021, 591(7848): 131-136. doi: 10.1038/s41586-021-03218-7
[32]	Zhan XM. Human parasitology[M]. 2nd ed. Beijing: People’s Medical Publishing House, 2010: 49-50, 96-102. (in Chinese)
	(詹希美. 人体寄生虫学[M]. 2版. 北京: 人民卫生出版社, 2010: 49-50, 96-102.)
[33]	Gorfu G, Cirelli KM, Melo MB, et al. Dual role for inflammasome sensors NLRP1 and NLRP3 in murine resistance to Toxoplasma gondii[J]. mBio, 2014, 5(1): e01117-13.
[34]	Pazoki H, Mohammad Rahimi H, Mirjalali H, et al. Soluble total antigen derived from Toxoplasma gondii tachyzoites increased the expression levels of NLRP1, NLRP3, NLRC4, AIM2, and the release of mature form of IL1β, but downregulated the expression of IL1β and IL18 genes in THP-1 cell line[J]. Microb Pathog, 2021, 158: 105072.
[35]	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): e12435.
[36]	Silva ALN, Santos LL, et al. Macrophage priming is dispensable for NLRP3 inflammasome activation and restriction of Leishmania amazonensis replication[J]. J Leukoc Biol, 2019, 106(3): 631-640. doi: 10.1002/JLB.MA1118-471R
[37]	Kihel A, Hammi I, Darif D, et al. The different faces of the NLRP3 inflammasome in cutaneous leishmaniasis: a review[J]. Cytokine, 2021, 147:155248.
[38]	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.e6. doi: S1931-3128(17)30538-3 pmid: 29290574
[39]	Rosazza T, Lecoeur H, Blisnick T, et al. Dynamic imaging reveals surface exposure of virulent Leishmania amastigotes during pyroptosis of infected macrophages[J]. J Cell Sci, 2020, 134(5): jcs242776.
[40]	Carvalho AM, Bacellar O, Carvalho EM. Protection and pathology in Leishmania braziliensis infection[J]. Pathogens, 2022, 11(4): 466. doi: 10.3390/pathogens11040466
[41]	Ashley EA, Pyae Phyo A, Woodrow CJ. Malaria[J]. Lancet, 2018, 391(10130): 1608-1621. doi: S0140-6736(18)30324-6 pmid: 29631781
[42]	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.
[43]	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
[44]	Otterdal K, Berg A, Michelsen AE, et al. IL-18 and IL-18 binding protein are related to disease severity and parasitemia during falciparum malaria[J]. BMC Infect Dis, 2021, 21(1): 1073. doi: 10.1186/s12879-021-06751-y pmid: 34663245
[45]	World Health Organization. Chagas disease (American trypanosomiasis) (2022)[EB/OL]. (2022-04-13) [2022-05-23]. https://www.who.int/news-room/fact-sheets/detail/chagas-disease-(american-trypanosomiasis).
[46]	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.
[47]	Paroli AF, Gonzalez PV, Díaz-Luján C, et al. NLRP3 inflammasome and caspase-1/11 pathway orchestrate different outcomes in the host protection against Trypanosoma cruzi acute infection[J]. Front Immunol, 2018, 9: 913. doi: 10.3389/fimmu.2018.00913
[48]	Medeiros NI, Pinto BF, Elói-Santos SM, et al. Evidence of different IL-1β activation pathways in innate immune cells from indeterminate and cardiac patients with chronic chagas disease[J]. Front Immunol, 2019, 10: 800. doi: 10.3389/fimmu.2019.00800 pmid: 31057540
[49]	Jasni N, Saidin S, Kin WW, et al. Entamoeba histolytica: membrane and non-membrane protein structure, function, immune response interaction, and vaccine development[J]. Membranes, 2022, 12(11): 1079. doi: 10.3390/membranes12111079
[50]	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.
[51]	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
[52]	Collaborative group on infectious diseases of obstetrics and gynecology branch of Chinese medical association. Diagnosis and treatment guidelines for trichomoniasis(2021 revised edition)[J]. Chin J Obstet Gynecol, 2021, 56(1): 7-10. (in Chinese)
	中华医学会妇产科学分会感染性疾病协作组. 阴道毛滴虫病诊治指南(2021修订版)[J]. 中华妇产科杂志, 2021, 56(1): 7-10.)
[53]	Riestra AM, Valderrama JA, Patras KA, et al. Trichomonas vaginalis induces NLRP3 inflammasome activation and pyroptotic cell death in human macrophages[J]. J Innate Immun, 2019, 11(1): 86-98. doi: 10.1159/000493585
[54]	Yadav S, Verma V, Dhanda RS, et al. Latent upregulation of Nlrp3, Nlrc4 and Aim2 differentiates between asymptomatic and symptomatic Trichomonas vaginalis infection[J]. Immunol Invest, 2022, 51(5): 1127-1148. doi: 10.1080/08820139.2021.1909062
[55]	Jiang YY, Ren JH, Yuan ZY, et al. Cryptosporidium andersoni as a novel predominant Cryptosporidium species in outpatients with diarrhea in Jiangsu Province, China[J]. BMC Infect Dis, 2014, 14: 555. doi: 10.1186/s12879-014-0555-7
[56]	Sateriale A, Gullicksrud JA, Engiles JB, et al. The intestinal parasite Cryptosporidium is controlled by an enterocyte intrinsic inflammasome that depends on NLRP6[J]. Proc Natl Acad Sci USA, 2021, 118(2): e2007807118.
[57]	Liu L, Yang YW, Fang R, et al. Giardia duodenalis and its secreted PPIB trigger inflammasome activation and pyroptosis in macrophages through TLR4-induced ROS signaling and A20-mediated NLRP3 deubiquitination[J]. Cells, 2021, 10(12): 3425. doi: 10.3390/cells10123425
[58]	Deplazes P, Rinaldi L, Alvarez Rojas CA, et al. Global distribution of alveolar and cystic echinococcosis[J]. Adv Parasitol, 2017, 95: 315-493.
[59]	Casulli A, Barth TFE, Tamarozzi F. Echinococcus multilocularis[J]. Trends Parasitol, 2019, 35(9): 738-739. doi: S1471-4922(19)30109-6 pmid: 31182385
[60]	Pan XB, Wang HB, Wang ZX, et al. Study on the expression level of NLRP3 inflammasome in hepatic alveolar echinococcosis[J]. Chin J Hepatobiliary Surg, 2020, 26(10): 753-756. (in Chinese)
	(潘徐彪, 王宏宾, 王志鑫, 等. NLRP3炎性小体在肝泡型包虫病中表达水平的研究[J]. 中华肝胆外科杂志, 2020(10): 753-756.)
[61]	Wang T. Expression and significance of focal death related factors such as GSDMD/Caspase-1, Caspase-4 and Caspase-5 in hepatic multilocular echinococcosis[D]. Xi ning: Qinghai university, 2019: 8-13. (in Chinese)
	(王涛. GSDMD/Caspase-1、Caspase-4、 Caspase-5等焦亡相关因子在肝多房包虫病的表达及其意义[D]. 西宁: 青海大学, 2019: 8-13.)
[62]	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. doi: 10.1073/pnas.1010337107
[63]	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): 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): 322-326.)
[64]	Wei LY, Jiang AQ, Jiang R, et al. Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization[J]. Innate Immun, 2021, 27(4): 313-323. doi: 10.1177/17534259211013397
[65]	Chen T, Cheng PC, Chang KC, et al. Activation of the NLRP3 and AIM2 inflammasomes in a mouse model of Schistosoma mansoni infection[J]. J Helminthol, 2019, 94: 1-9.

细胞焦亡在人体寄生虫病中的研究进展

Research progress on the role of pyroptosis in human parasitic diseases

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[1]	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.
[2]	温镇成, 季小芳, 林桂莹, 汤娟娟, 王漫妮, 梁翠莹, 肖林卓, 李孜*. 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.
[3]	林金祥. 近年福建省人体寄生虫病流行状况的变化[J]. 中国寄生虫学与寄生虫病杂志, 2003, 21(5): 18-319.
[4]	. 河北省寄生虫病防治工作总结[J]. 中国寄生虫学与寄生虫病杂志, 1995, 13(S1): 86-88.
[5]	. 广东省寄生虫病“八五”防治规划1991—1993年执行情况[J]. 中国寄生虫学与寄生虫病杂志, 1995, 13(S1): 121-124.
[6]	顿珠. 预防为主、因地制宜、为实现寄生虫病防治目标而努力[J]. 中国寄生虫学与寄生虫病杂志, 1995, 13(S1): 155-156.
[7]	余森海,许隆祺,蒋则孝,徐淑惠,韩家俊,朱育光,常江,林金祥,徐伏牛. 首次全国人体寄生虫分布调查总结[J]. 中国寄生虫学与寄生虫病杂志, 1994, 12(S1): 2-7.
[8]	吴月华,吴献洪,郭在宣,马明跃,王晓胜,袁小明,安少军. 青海省格尔木市人群寄生虫感染情况的调查[J]. 中国寄生虫学与寄生虫病杂志, 1994, 12(S1): 244-244.
[9]	苏文明,凌文武,何启富,黄荣英,陈德义,林永健. 广西田阳县人群寄生虫感染情况的调查[J]. 中国寄生虫学与寄生虫病杂志, 1994, 12(S1): 248-249.
[10]	董吉生,莫文安. 广西钟山县人群寄生虫感染情况的调查[J]. 中国寄生虫学与寄生虫病杂志, 1994, 12(S1): 249-249.
[11]	师全仁,张巧玲,马成骥,刚美琳. 宁夏平罗县人群寄生虫感染情况的调查[J]. 中国寄生虫学与寄生虫病杂志, 1991, 9(S1): 154-155.
[12]	吴刚(?),李方印. 山西省芮城县人群寄生虫感染情况的调查[J]. 中国寄生虫学与寄生虫病杂志, 1991, 9(S1): 162-163.
[13]	余森海,蒋则孝,许隆祺. 我国人体寄生虫病流行现状[J]. 中国寄生虫学与寄生虫病杂志, 1988, 6(S1): 9-9.
[14]	蒋则孝. 全国人体寄生虫分布调查方法标准化讲习班在成都举行[J]. 中国寄生虫学与寄生虫病杂志, 1986, 4(4): 312-312.
[15]	. 新书介绍[J]. 中国寄生虫学与寄生虫病杂志, 1986, 4(2): 153-153.