阻断半乳糖凝集素-受体相互作用对弓形虫感染小鼠小肠免疫病理的影响

doi:10.12140/j.issn.1000-7423.2023.03.003

中国寄生虫学与寄生虫病杂志 ›› 2023, Vol. 41 ›› Issue (3): 279-285.doi: 10.12140/j.issn.1000-7423.2023.03.003

阻断半乳糖凝集素-受体相互作用对弓形虫感染小鼠小肠免疫病理的影响

欧阳然¹(), 刘星卓¹, 黄世光²^,³, 吕芳丽¹^,⁴^,⁵^,⁶^,^*()

1 中山大学中山医学院寄生虫学教研室，广东广州 510080
2 深圳南油麦芽口腔门诊部，广东深圳 518067
3 暨南大学口腔医学院，广东广州 511468
4 中山大学附属第七医院检验科，广东深圳 518107
5 中山大学医学院寄生虫学教研室，广东深圳 518107
6 中山大学热带病防治研究教育部重点实验室，广东广州 510080

收稿日期:2022-09-16 修回日期:2023-02-08 出版日期:2023-06-30 发布日期:2023-06-28
通讯作者: *吕芳丽，女，博士，教授，从事寄生虫感染免疫研究。E-mail：lvfangli@mail.sysu.edu.cn
作者简介:欧阳然（1999-），女，本科，从事弓形虫致病机制研究。E-mail：949817833@qq.com
基金资助:
国家自然科学基金面上项目(82272366);国家自然科学基金面上项目(81971955);广东省自然科学基金面上项目(2021A1515012115);广东省自然科学基金面上项目(2019A1515011667);深圳市自然科学基金面上项目(JCYJ20220530145002006);广东省研究生教育创新计划项目(2021SFKC003);中山大学校级本科教学质量工程项目（中大教务[2022]91号）;中山大学校级本科教学质量工程项目（中大教务[2021]93号）

Effect of locking galectin-receptor interaction on the immunopathology of small intestine of Toxoplasma gondii-infected mice

OU Yangran¹(), LIU Xingzhuo¹, HUANG Shiguang²^,³, LYU Fangli¹^,⁴^,⁵^,⁶^,^*()

1 Department of Parasitology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, Guangdong, China
2 Shenzhen Nanyou Malt Dentistry Out-patient Department, Shengzhen 518067, Guangdong, China
3 School of Stomatology, Jinan University, Guangzhou 511468, Guangdong, China
4 Department of Clinical Laboratory, the Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen 518107, Guangdong, China
5 Department of Parasitology, School of Medicine, Sun Yat-sen University, Shenzhen 518107, Guangdong, China
6 Key Laboratory of Tropical Disease of the Ministry of Education, Sun Yat-sen University, Guangzhou 510080, Guangdong, China

Received:2022-09-16 Revised:2023-02-08 Online:2023-06-30 Published:2023-06-28
Contact: *E-mail: lvfangli@mail.sysu.edu.cn
Supported by:
National Natural Science Foundation of China(82272366);National Natural Science Foundation of China(81971955);Natural Science Foundation of Guangdong Province(2021A1515012115);Natural Science Foundation of Guangdong Province(2019A1515011667);Shenzhen Municipal Natural Science Foundation(JCYJ20220530145002006);Graduate Education Innovation Plan Project of Guangdong Province(2021SFKC003);Undergraduate Teaching Quality Engineering Project of Sun Yat-sen University (SYSU Undergraduate Education [2022]91);Undergraduate Teaching Quality Engineering Project of Sun Yat-sen University (SYSU Undergraduate Education [2022]93)

摘要/Abstract

摘要：

目的探讨半乳糖凝集素与受体的相互作用对弓形虫感染小鼠小肠免疫病理的调节作用。方法将18只雌性BALB/c小鼠随机分成4组：未感染组（naive组）4只、α-乳糖组（lactose组）4只、弓形虫感染组（Tg组）5只和弓形虫感染+lactose组（Tg+lactose组）5只。Tg组和Tg+lactose组每鼠腹腔注射约1 000个弓形虫速殖子，naive组和lactose组腹腔注射PBS 0.2 ml。感染后当天开始，Tg+lactose组和lactose组每鼠腹腔注射0.2 mol/L的lactose 0.2 ml，naive组和Tg组每鼠腹腔注射等体积的PBS，早、晚各1次，连续注射7 d。感染弓形虫后，记录各组小鼠的生存时间。在感染后第7天处死小鼠，取空肠中段进行石蜡切片和HE染色，观察小鼠小肠组织的病理变化；取小鼠空肠下段提总RNA后逆转录，以β肌动蛋白（β-actin）作为内参基因，qRT-PCR检测小鼠小肠组织弓形虫表面抗原1（SAG1）、半乳糖凝集素3（galectin-3）、galectin-9、T细胞免疫球蛋白黏蛋白-3（Tim-3）、白细胞分化抗原137（CD137）、白细胞介素12（IL-12）、γ-干扰素（IFN-γ）、IL-10、IL-4、转化生长因子β（TGF-β）、趋化因子受体2（CCR2）、和几丁质酶3样分子3（Ym1）的mRNA相对表达水平。结果感染弓形虫后，naive组和lactose组小鼠无死亡，Tg组小鼠的存活时间为182~188 h，Tg+lactose组小鼠的存活时间为180~182 h；两组小鼠的生存时间差异有统计学意义（χ² = 19.52，P < 0.05）。HE染色结果显示，naive组和lactose组小鼠的空肠组织未观察到炎症改变；Tg组和Tg+lactose组小鼠的小肠组织观察到肠绒毛缩短，肠隐窝变浅，绒毛顶端上皮细胞坏死，小肠黏膜组织中有炎症细胞浸润。与Tg组的相比，Tg+lactose组小鼠小肠组织的病理损伤更加严重。qRT-PCR结果显示，Tg+lactose组小鼠小肠组织SAG1的mRNA相对表达水平为9.17 ± 1.65，高于Tg组的1.00 ± 0.84（t = 4.40，P < 0.05）。naive组、lactose组、Tg组和Tg+lactose组小鼠小肠组织galectin-3的mRNA相对表达水平分别为1.00 ± 0.28、1.71 ± 0.31、2.46 ± 1.11和7.10 ± 1.57（F = 10.15，P < 0.01），galectin-9的mRNA相对表达水平分别为1.00 ± 0.31、1.44 ± 0.26、3.21 ± 1.01和7.00 ± 1.08（F = 14.53，P < 0.01），Tim-3的mRNA相对表达水平分别为1.00 ± 0.12、0.88 ± 0.28、1.64 ± 0.31和4.89 ± 0.69（F = 19.15，P < 0.01），CD137的mRNA相对表达水平分别为1.00 ± 0.42、1.03 ± 0.30、0.89 ± 0.11和3.84 ± 0.77（F = 8.46，P < 0.01），IL-12的mRNA相对表达水平分别为1.00 ± 0.35、1.14 ± 0.56、12.37 ± 4.43和18.42 ± 3.89（F = 10.18，P < 0.01），IFN-γ的mRNA相对表达水平分别为1.00 ± 0.56、1.65 ± 0.53、5.57 ± 1.84和21.26 ± 6.48（F = 10.38，P < 0.01），IL-10的mRNA相对表达水平分别为1.00 ± 0.20、1.10 ± 0.25、8.65 ± 2.52和21.98 ± 3.96（F = 20.84，P < 0.01）。小鼠小肠组织中IL-4、TGF-β和CCR2的mRNA相对表达水平在naive组、lactose组、Tg组和Tg+lactose组之间差异无统计学意义（F = 1.09、4.74、2.03，均P > 0.05）。naive组和lactose组未检测到Ym1的mRNA表达，Tg组和Tg+lactose组Ym1的mRNA相对表达水平差异无统计学意义（t = 0.24，P > 0.05）。结论阻断半乳糖凝集素-受体相互作用后，弓形虫感染小鼠的小肠组织虫荷增加、病理损伤加重，galectin-3、galectin-9、Tim-3、CD137、IL-10和IFN-γ的表达上调。

关键词: 弓形虫, 感染小鼠, 小肠, 半乳糖凝集素

Abstract:

Objective To investigate the regulatory effect of galectin-receptor interaction on the small intestine immunopathology of Toxoplasma gondii-infected mice. Methods Eighteen female BALB/c mice were randomly divided into 4 groups: 4 mice in uninfected group (naive group), 4 mice in lactose group (lactose group), 5 mice in T. gondii infection group (Tg group) and 5 mice in T. gondii infection + lactose group (Tg+lactose group). Each mouse in the Tg group and the Tg+lactose group was intraperitoneally (i.p.) injected with 1 000 tachyzoites of T. gondii RH strain, while the naive group and lactose group were i.p. injected with 0.2 ml PBS. Starting from day 0 post infection, each mouse in the Tg+lactose group and the lactose group was i.p. injected with 0.2 ml 0.2 mol/L of lactose, while each mouse in the naive group and the Tg group was i.p. injected with an equal volume of PBS, once in the morning and once in the evening for 7 consecutive days. After infection with T. gondii, the mice survival time in each group was recorded. The mice were euthanized on the 7th day after infection to collect middle segment of jejunum from each mouse for prepareing paraffin sections, which were stained with hematoxylin and eosin (HE) to observe the pathological changes; from the lower segment of jejunum of each mouse, total RNA was extracted and reverse-transcribed, and used in quantitative real-time reverse transcription PCR (qRT-PCR) with β-actin as an internal reference gene to detect the relative mRNA expression level of surface antigen 1 (SAG1), galectin-3, galectin-9, T cell immunoglobulin mucin 3 (Tim-3), leukocyte differentiation antigen 137 (CD137), interleukin 12 (IL-12), interferon-γ (IFN-γ), IL-10, IL-4, transforming growth factor β (TGF-β), chemokine receptor 2 (CCR2) and chitinase 3 like molecule 3 (Ym1). Results After infection with T. gondii, there was no mice died in the naive group and the lactose group. The survival time of the mice in the Tg group was 182-188 h, and the survival time of the mice in the Tg+lactose group was 180-182 h; the difference of the survival time between the two groups was statistically significant (χ² = 19.52, P < 0.05). HE staining showed no inflammation in the mice jejunal tissue in the naive group and lactose group. Shortened intestinal villus, shallower intestinal crypts, necrosis of epithelial cells at the top of villi and inflammatory cell infiltration in the intestinal mucosa were observed in the mice small intestine from the Tg group and Tg+lactose group. Compared with the Tg group, the pathological change of the mice small intestine in the Tg+lactose group was more severe. The qRT-PCR results showed that the relative mRNA expression of SAG1 in the mice small intestine of the Tg+lactose group was 9.17 ± 1.65, which was higher than that in the Tg group (1.00 ± 0.84, t = 4.40, P < 0.05). The relative mRNA expression levels of galectin-3 in the mce small intestine of the naive group, lactose group, Tg group, and Tg+lactose group were 1.00 ± 0.28, 1.71 ± 0.31, 2.46 ± 1.11, and 7.10 ± 1.57, respectively (F = 10.15, P < 0.01). The mRNA expression levels of galectin-9 in the 4 groups were 1.00 ± 0.31, 1.44 ± 0.26, 3.21 ± 1.01, and 7.00 ± 1.08, respectively (F = 14.53, P < 0.01). The mRNA expression levels of Tim-3 in the 4 groups were 1.00 ± 0.12, 0.88 ± 0.28, 1.64 ± 0.31, and 4.89 ± 0.69, respectively (F = 19.15, P < 0.01). The mRNA expression levels of CD137 in the 4 groups were 1.00 ± 0.42, 1.03 ± 0.30, 0.89 ± 0.11, and 3.84 ± 0.77, respectively (F = 8.46, P < 0.01). The mRNA expression levels of IL-12 in the 4 groups were 1.00 ± 0.35, 1.14 ± 0.56, 12.37 ± 4.43, and 18.42 ± 3.89, respectively (F = 10.18, P < 0.01). The mRNA expression levels of IFN-γ in the 4 groups were 1.00 ± 0.56, 1.65 ± 0.53, 5.57 ± 1.84, and 21.26 ± 6.48, respectively (F = 10.38, P < 0.01). The mRNA expression levels of IL-10 in the 4 groups were 1.00 ± 0.20, 1.10 ± 0.25, 8.65 ± 2.52, and 21.98 ± 3.96, respectively (F = 20.84, P < 0.01). The mRNA expression levels of IL-4, TGF-β, and CCR2 in the mice small intestine among the naive group, lactose group, Tg group, and Tg+lactose group had no statistically significant differences (F = 1.09, 4.74, and 2.03, P > 0.05). Ym1 mRNA expression was not detected in the naive group and lactose group, and Ym1 mRNA expression levels between the Tg group and the Tg+lactose group had no statistically significant difference (t = 0.24, P > 0.05). Conclusion Blockage of galectins-receptor interaction in mice infected with T. gondii leads to increased parasite burden in small intesting tissues, and aggravated pathological impairment, as well as upregulated expression of galectin-3, galectin-9, Tim-3, CD137, IL-10 and IFN-γ.

Key words: Toxoplasma gondii, Infected mice, Small intestine, Galectin

中图分类号:

R531.8

欧阳然, 刘星卓, 黄世光, 吕芳丽. 阻断半乳糖凝集素-受体相互作用对弓形虫感染小鼠小肠免疫病理的影响[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(3): 279-285.

OU Yangran, LIU Xingzhuo, HUANG Shiguang, LYU Fangli. Effect of locking galectin-receptor interaction on the immunopathology of small intestine of Toxoplasma gondii-infected mice[J]. Chinese Journal of Parasitology and Parasitic Diseases, 2023, 41(3): 279-285.

图/表 5

表1

图1

图2

图3

图4

参考文献 27

[1]	Wu YP, Ji TK, Bai SY, et al. Progress in diagnosis of toxoplasmosis[J]. Chin J Am Infect Dis, 2021, 1-17. (in Chinese)
	(吴云萍, 祭天锴, 白邵缘, 等. 弓形虫病诊断研究进展[J]. 中国动物传染病学报, 2021, 1-17.)
[2]	Jones JL, Kruszon-Moran D, Sanders-Lewis K, et al. Toxoplasma gondii infection in the United States, 1999—2004, decline from the prior decade[J]. Am J Trop Med Hyg, 2007, 77(3): 405-410.
[3]	Snyder LM, Denkers EY. From initiators to effectors: roadmap through the intestine during encounter of Toxoplasma gondii with the mucosal immune system[J]. Front Cell Infect Microbiol, 2020, 10: 614701.
[4]	Gazzinelli RT, Hieny S, Wynn TA, et al. Interleukin 12 is required for the T-lymphocyte-independent induction of interferon gamma by an intracellular parasite and induces resistance in T-cell-deficient hosts[J]. Proc Natl Acad Sci USA, 1993, 90(13): 6115-6119.
[5]	Hunter CA, Subauste CS, Van Cleave VH, et al. Production of gamma interferon by natural killer cells from Toxoplasma gondii-infected SCID mice: regulation by interleukin-10, interleukin-12, and tumor necrosis factor alpha[J]. Infect Immun, 1994, 62(7): 2818-2824.
[6]	Shi WK, Xue CY, Su XZ, et al. The roles of galectins in parasitic infections[J]. Acta Trop, 2018, 177: 97-104.
[7]	Nio-Kobayashi J. Histological mapping and subtype-specific functions of galectins in health and disease[J]. Trends Glycosci Glycotechnol, 2018, 30(172): SJ47-SJ53.
[8]	Gao ZY, Liu ZN, Wang R, et al. Galectin-3 is a potential mediator for atherosclerosis[J]. J Immunol Res, 2020, 2020: 5284728.
[9]	Dong R, Zhang M, Hu QY, et al. Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review)[J]. Int J Mol Med, 2018, 41(2): 599-614.
[10]	Vasta GR. Roles of galectins in infection[J]. Nat Rev Microbiol, 2009, 7(6): 424-438.
[11]	Wu YF, Lyu FL. Galectin-receptor interactions on the regulation of small intestinal pathology of Plasmodium berghei-infected mice[J]. J Trop Med, 2019, 19(5): 541-544. (in Chinese)
	(吴一凡, 吕芳丽. 半乳糖凝集素-受体相互作用对感染伯氏疟原虫小鼠小肠病理的调节[J]. 热带医学杂志, 2019, 19(5): 541-544.)
[12]	Yan JH, Lyu FL. The galectin-receptor interaction may regulate intestinal mucosal immunity of mice infected with Trichinella spiralis[J]. J Trop Med, 2021, 21(5): 540-543, 622. (in Chinese)
	(颜景海, 吕芳丽. 半乳糖凝集素-受体相互作用对旋毛虫感染小鼠肠道黏膜免疫的调节[J]. 热带医学杂志, 2021, 21(5): 540-543, 622.)
[13]	Lee JN, Kim J, Lee JH, et al. SIRT1 promotes host protective immunity against Toxoplasma gondii by controlling the FoxO-autophagy axis via the AMPK and PI3K/AKT signalling pathways[J]. Int J Mol Sci, 2022, 23(21): 13578.
[14]	Zhang YX, He J, Zheng HQ, et al. Association of TREM-1, IL-1β, IL-33/ST2, and TLR expressions with the pathogenesis of ocular toxoplasmosis in mouse models on different genetic backgrounds[J]. Front Microbiol, 2019, 10: 2264.
[15]	Bernardes ES, Silva NM, Ruas LP, et al. Toxoplasma gondii infection reveals a novel regulatory role for galectin-3 in the interface of innate and adaptive immunity[J]. Am J Pathol, 2006, 168(6): 1910-1920.
[16]	Zhu C, Anderson AC, Schubart A, et al. The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity[J]. Nat Immunol, 2005, 6(12): 1245-1252.
[17]	Bitra A, Doukov T, Wang J, et al. Crystal structure of murine 4-1BB and its interaction with 4-1BBL support a role for galectin-9 in 4-1BB signaling[J]. J Biol Chem, 2018, 293(4): 1317-1329.
[18]	Eriksen LL, Nielsen MA, Laursen TL, et al. Early loss of T lymphocyte 4-1BB receptor expression is associated with higher short-term mortality in alcoholic hepatitis[J]. PLoS One, 2021, 16(8): e0255574.
[19]	He J, Hou YH, Lu FL. Blockage of galectin-receptor interactions attenuates mouse hepatic pathology induced by Toxoplasma gondii infection[J]. Front Immunol, 2022, 13: 896744.
[20]	Hu XH, Tang MX, Mor G, et al. Tim-3: Expression on immune cells and roles at the maternal-fetal interface[J]. J Reprod Immunol, 2016, 118: 92-99.
[21]	Wu C, Thalhamer T, Franca RF, et al. Galectin-9-CD44 interaction enhances stability and function of adaptive regulatory T cells[J]. Immunity, 2014, 41(2): 270-282.
[22]	Raetz M, Hwang SH, Wilhelm CL, et al. Parasite-induced TH1 cells and intestinal dysbiosis cooperate in IFN-γ-dependent elimination of Paneth cells[J]. Nat Immunol, 2013, 14(2): 136-142.
[23]	Heimesaat MM, Bereswill S, Fischer A, et al. Gram-negative bacteria aggravate murine small intestinal Th1-type immunopathology following oral infection with Toxoplasma gondii[J]. J Immunol, 2006, 177(12): 8785-8795.
[24]	Wu B, Lyu FL. Progress of CD8⁺ T cell-mediated immune response to Toxoplasma gondii infection[J]. Chin J Parasitol Parasit Dis, 2014, 32(2): 143-147. (in Chinese)
	(吴斌, 吕芳丽. CD8⁺ T细胞免疫应答在刚地弓形虫感染免疫中的功能研究进展[J]. 中国寄生虫学与寄生虫病杂志, 2014, 32(2): 143-147.)
[25]	Lang C, Gross U, Lüder CGK. Subversion of innate and adaptive immune responses by Toxoplasma gondii[J]. Parasitol Res, 2007, 100(2): 191-203.
[26]	Kobayashi M, Aosai F, Hata H, et al. Toxoplasma gondii: difference of invasion into tissue of digestive organs between susceptible and resistant strain and influence of IFN-gamma in mice inoculated with the cysts perorally[J]. J Parasitol, 1999, 85(5): 973-975.
[27]	Shin EH, Chun YS, Kim WH, et al. Immune responses of mice intraduodenally infected with Toxoplasma gondii KI-1 tachyzoites[J]. Korean J Parasitol, 2011, 49(2): 115-123.

基因名称 Genes name	引物序列（5'→ 3'） Primer sequence(5'→ 3')	基因ID Gene ID
β⁃actin	F TGGAATCCTGTGGCATCCATGAAA	114610
β⁃actin	R TAAAACGCAGCTCAGTAACAGTCC	114610
SAG1	F CTGTAGCCTCGGAGGAAACACA	202150
SAG1	R GCCAGGTTTGTGTCCTCATGCT	202150
galectin⁃3	F AACACGAAGCAGGACAATAACTGG	168540
galectin⁃3	R GCAGTAGGTGAGCATCGTTGAC	168540
galectin⁃9	F CTGGAATCCCTCCTGTGGTGTA	168590
galectin⁃9	R CCTCGTAGCATCTGGCAAGACA	168590
Tim⁃3	F ACAGACACTGGTGACCCTCCAT	171285
Tim⁃3	R CAGCAGAGACTCCCACTCCAAT	171285
CD137	F CCAAGTACCTTCTCCAGCATAGG	219420
CD137	R GCGTTGTGGGTAGAGGAGCAAA	219420
IL⁃12	F ACGAGAGTTGCCTGGCTACTAG	161590
IL⁃12	R CCTCATAGATGCTACCAAGGCAC	161590
IFN⁃γ	F CAGCAACAGCAAGGCGAAAAAGG	159780
IFN⁃γ	R TTTCCGCTTCCTGAGGCTGGAT	159780
IL⁃10	F CGGGAAGACAATAACTGCACCC	161530
IL⁃10	R CGGTTAGCAGTATGTTGTCCAGC	161530
IL⁃4	F ATCATCGGCATTTTGAACGAGGTC	161890
IL⁃4	R ACCTTGGAAGCCCTACAGACGA	161890
TGF⁃β	F TGATACGCCTGAGTGGCTGTCT	218030
TGF⁃β	R CACAAGAGCAGTGAGCGCTGAA	218030
CCR2	F ATCCACGGCATACTATCAACATC	127720
CCR2	R CAAGGCTCACCATCATCGTAG	127720
Ym1	F CAGGTCTGGCAATTCTTCTGAA	126550
Ym1	R GTCTTGCTCATGTGTGTAAGTGA	126550

阻断半乳糖凝集素-受体相互作用对弓形虫感染小鼠小肠免疫病理的影响

Effect of locking galectin-receptor interaction on the immunopathology of small intestine of Toxoplasma gondii-infected mice

RichHTML

PDF (PC)

可视化

摘要/Abstract

引用本文

使用本文

图/表 5

参考文献 27

相关文章 15

编辑推荐

Metrics

本文评价

[1]	景天宇, 牟汝涛, 张帆, 刘现兵, 胡雪梅, 张海霞, 李志丹. 孕期刚地弓形虫感染对滋养层细胞和蜕膜免疫细胞表面CD73表达的影响及其与不良妊娠的关系[J]. 中国寄生虫学与寄生虫病杂志, 2025, 43(2): 210-216.
[2]	章孝成, 胡媛, 彭荟, 沈玉娟, 刘华, 曹建平. 基于CRISPR/Cas9技术的刚地弓形虫bfd2缺陷虫株的构建及表型分析[J]. 中国寄生虫学与寄生虫病杂志, 2025, 43(2): 217-222.
[3]	张铃, 刘星卓, 吕芳丽. 非洲刚地弓形虫感染和弓形虫病流行概况[J]. 中国寄生虫学与寄生虫病杂志, 2025, 43(2): 241-251.
[4]	殷荷, 马磊, 党甜甜, 李佳铭, 赵志军. 刚地弓形虫Ⅰ/Ⅲ型ROP16调控TAF15对THP-1细胞影响及机制研究[J]. 中国寄生虫学与寄生虫病杂志, 2025, 43(1): 103-111.
[5]	堵舒桐, 杨翼维, 吴恬菲. 2020—2022年大理恶性肿瘤患者血清抗弓形虫抗体调查[J]. 中国寄生虫学与寄生虫病杂志, 2024, 42(6): 806-809.
[6]	李仕毓, 李静, 陆绍红, 郑斌. 宿主细胞自主免疫抗弓形虫的研究进展[J]. 中国寄生虫学与寄生虫病杂志, 2024, 42(5): 653-658.
[7]	李静, 杨树峰, 高文伟, 刘卿, 朱兴全, 郑文斌. 山西省晋中市猪刚地弓形虫的感染情况及基因型鉴定[J]. 中国寄生虫学与寄生虫病杂志, 2024, 42(3): 367-371.
[8]	解晓曼, 孙航, 代莉莎, 朱文菊, 王利磊, 谢环环, 董宏杰, 张俊梅, 王琦, 周贝贝, 赵桂华, 徐超, 尹昆. 刚地弓形虫感染对小鼠脑组织转录本m⁶A甲基化修饰的影响[J]. 中国寄生虫学与寄生虫病杂志, 2024, 42(1): 27-35.
[9]	郑广福, 刘现兵, 姜昱竹, 李新雨, 胡雪梅, 张海霞. 刚地弓形虫感染孕鼠胎盘组织中中性粒细胞和IL-17与不良妊娠结局的关系[J]. 中国寄生虫学与寄生虫病杂志, 2024, 42(1): 48-54.
[10]	薛羽珊, 林萍, 程训佳, 冯萌. 慢性弓形虫感染对宿主中枢神经系统的损伤及其作用机制[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(5): 527-531.
[11]	姜文静, 孟雅莉, 赵利娜, 王春苗, 张晓磊. 刚地弓形虫棒状体蛋白18和膜表面抗原30复合核酸疫苗对小鼠的免疫保护作用[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(5): 532-538.
[12]	赵紫琪, 吕芳丽. 蒿甲醚脂质体体外抑制刚地弓形虫增殖作用的研究[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(4): 446-451.
[13]	张驰, 陈嘉婷, 辛紫萱, 杨莉莉, 杨梓瀚, 彭鸿娟. 弓形虫慢性感染小鼠脑转录组分析及与抑郁相关的犬尿氨酸通路的验证[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(3): 270-278.
[14]	杜鹃, 李佳, 吴迪, 余琦, 张玮, 白如念, 郭俊林, 刘庆斌, 雷琪莉, 谷传慧, 王萌, 赵浩军. 2022年北京市犬猫刚地弓形虫感染血清流行病学调查[J]. 中国寄生虫学与寄生虫病杂志, 2023, 41(3): 389-392.
[15]	李佳铭, 王艺璇, 杨宁爱, 马慧慧, 兰敏, 刘春兰, 赵志军. 刚地弓形虫ROP16蛋白对MH-S细胞极化和凋亡的影响及其相关机制[J]. 中国寄生虫学与寄生虫病杂志, 2022, 40(5): 579-586.