Parasites, Hosts and Diseases

"IL-10"

Original Articles

Trichomonas vaginalis α-Actinin 2 Modulates Host Immune Responses by Inducing Tolerogenic Dendritic Cells via IL-10 Production from Regulatory T Cells: Hye-Yeon Lee, Juri Kim, Jae-Sook Ryu, Soon-Jung Park; Korean J Parasitol 2017;55(4):375-384.
Published online August 31, 2017; DOI: https://doi.org/10.3347/kjp.2017.55.4.375

Abstract
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Trichomonas vaginalis is a pathogen that triggers severe immune responses in hosts. T. vaginalis α-actinin 2, Tvα-actinin 2, has been used to diagnose trichomoniasis. This study was undertaken to examine the role of Tvα-actinin 2 as an antigenic molecule to induce immune responses from humans. Western blot analysis using anti-Tvα-actinin 2 antibodies indicated its presence in the secreted proteins of T. vaginalis. ELISA was employed to measure cytokine production by vaginal epithelial cells, prostate cells, mouse dendritic cells (DCs), or T cells stimulated with T. vaginalis or Tvα-actinin 2 protein. Both T. vaginalis and rTvα-actinin 2 induced cytokine production from epithelial cell lines, including IL-10. Moreover, CD4⁺CD25^- regulatory T cells (Treg cells) incubated with rTvα-actinin 2-treated DCs produced high levels of IL-10. These data indicate that Tvα-actinin 2 modulates immune responses via IL-10 production by Treg cells.

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Identification and Characterization of α-Actinin 1 of Histomonas meleagridis and Its Potential Vaccine Candidates against Histomonosis
Dandan Liu, Chen Chen, Qiaoguang Chen, Shuang Wang, Zaifan Li, Jie Rong, Yuming Zhang, Zhaofeng Hou, Jianping Tao, Jinjun Xu
Animals.2023; 13(14): 2330. CrossRef
Surface‐enhanced Raman scattering of secretory proteins for the cytotoxicity analysis of low‐dose doxorubicin
Mengmeng Zheng, Siqi Gao, Yamin Lin, Yating Lin, Zufang Huang, Shusen Xie, Yun Yu, Juqiang Lin
Journal of Raman Spectroscopy.2020; 51(11): 2217. CrossRef
Vasoactive intestinal peptide is required in the maintenance of immune regulatory competency of immune regulatory monocytes
L Guan, D Yu, G-H Wu, H-J Ning, S-D He, S-S Li, T-Y Hu, G Yang, Z-Q Liu, H-Q Yu, X-Z Sun, Z-G Liu, P-C Yang
Clinical and Experimental Immunology.2019; 196(2): 276. CrossRef

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Low Fetal Weight is Directly Caused by Sequestration of Parasites and Indirectly by IL-17 and IL-10 Imbalance in the Placenta of Pregnant Mice with Malaria: Loeki Enggar Fitri, Teguh Wahju Sardjono, Zainabur Rahmah, Budi Siswanto, Kusworini Handono, Yoes Prijatna Dachlan; Korean J Parasitol 2015;53(2):189-196.
Published online April 22, 2015; DOI: https://doi.org/10.3347/kjp.2015.53.2.189

Abstract
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The sequestration of infected erythrocytes in the placenta can activate the syncytiotrophoblast to release cytokines that affect the micro-environment and influence the delivery of nutrients and oxygen to fetus. The high level of IL-10 has been reported in the intervillous space and could prevent the pathological effects. There is still no data of Th17 involvement in the pathogenesis of placental malaria. This study was conducted to reveal the influence of placental IL-17 and IL-10 levels on fetal weights in malaria placenta. Seventeen pregnant BALB/C mice were divided into control (8 pregnant mice) and treatment group (9 pregnant mice infected by Plasmodium berghei). Placental specimens stained with hematoxylin and eosin were examined to determine the level of cytoadherence by counting the infected erythrocytes in the intervillous space of placenta. Levels of IL-17 and IL-10 in the placenta were measured using ELISA. All fetuses were weighed by analytical balance. Statistical analysis using Structural Equation Modeling showed that cytoadherence caused an increased level of placental IL-17 and a decreased level of placental IL-10. Cytoadherence also caused low fetal weight. The increased level of placental IL-17 caused low fetal weight, and interestingly low fetal weight was caused by a decrease of placental IL-10. It can be concluded that low fetal weight in placental malaria is directly caused by sequestration of the parasites and indirectly by the local imbalance of IL-17 and IL-10 levels.

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Graziella Rubino, Efdal Yörük
Transplant Immunology.2024; 86: 102068. CrossRef
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Subulade A. Ademola, Oluwayemi J. Bamikole, Olukemi K. Amodu
Frontiers in Immunology.2023;[Epub] CrossRef
Interleukin-17 promotes proliferation, migration, and invasion of trophoblasts via regulating PPAR-γ/RXR-α/Wnt signaling
Zhuo Zhang, Yuhua Yang, Xiaomei Lv, Hongyuan Liu
Bioengineered.2022; 13(1): 1224. CrossRef
Pregnancy-associated malaria: Effects of cytokine and chemokine expression
Karen E. Sánchez, Lilian M. Spencer
Travel Medicine and Infectious Disease.2022; 47: 102282. CrossRef
Malaria and pregnancy: a Venezuelan approach. Review article
Daniel Ernesto Carvallo Ruiz, Elizabeth Natalia Martínez-Núñez, José Manuel Martín-Castelli, Samantha Margaret Arrizabalo-Seir, Aixa Guadalupe Medina-Gamboa, José Núñez-Troconis
Obstetrics & Gynecology International Journal.2022; 13(5): 311. CrossRef
Impact of placental malaria on maternal, placental and fetal cord responses and its role in pregnancy outcomes in women from Blue Nile State, Sudan
Samia Omer, Clara Franco-Jarava, Ali Noureldien, Mona Omer, Mutasim Abdelrahim, Israel Molina, Ishag Adam
Malaria Journal.2021;[Epub] CrossRef
Establishing a conceptual framework of the impact of placental malaria on infant neurodevelopment
Harriet L.S. Lawford, Anne CC Lee, Sailesh Kumar, Helen G. Liley, Samudragupta Bora
International Journal of Infectious Diseases.2019; 84: 54. CrossRef
IL-10 producing B cells rescue mouse fetuses from inflammation-driven fetal death and are able to modulate T cell immune responses
Mandy Busse, Kim-Norina Jutta Campe, Desiree Nowak, Anne Schumacher, Susanne Plenagl, Stefanie Langwisch, Gisa Tiegs, Annegret Reinhold, Ana Claudia Zenclussen
Scientific Reports.2019;[Epub] CrossRef
Trichomonas vaginalis exosome‐like vesicles modify the cytokine profile and reduce inflammation in parasite‐infected mice
L. M. Olmos‐Ortiz, M. A. Barajas‐Mendiola, M. Barrios‐Rodiles, L. E. Castellano, S. Arias‐Negrete, E. E. Avila, P. Cuéllar‐Mata
Parasite Immunology.2017;[Epub] CrossRef
Malaria in pregnancy: the relevance of animal models for vaccine development
Justin Doritchamou, Andrew Teo, Michal Fried, Patrick E Duffy
Lab Animal.2017; 46(10): 388. CrossRef

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Parasitic Helminth Cystatin Inhibits DSS-Induced Intestinal Inflammation Via IL-10⁺F4/80⁺ Macrophage Recruitment: Sung Won Jang, Min Kyoung Cho, Mi Kyung Park, Shin Ae Kang, Byoung-Kuk Na, Soon Cheol Ahn, Dong-Hee Kim, Hak Sun Yu; Korean J Parasitol 2011;49(3):245-254.
Published online September 30, 2011; DOI: https://doi.org/10.3347/kjp.2011.49.3.245

Abstract
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Many immune down-regulatory molecules have been isolated from parasites, including cystatin (cystain protease inhibitor). In a previous study, we isolated and characterized Type I cystatin (CsStefin-1) of the liver fluke, Clonorchis sinensis. To investigate whether the CsStefin-1 might be a new host immune modulator, we induced intestinal inflammation in mice by dextran sodium sulfate (DSS) and treated them with recombinant CsStefin-1 (rCsStefin-1). The disease activity index (DAI) increased in DSS only-treated mice. In contrast, the DAI value was significantly reduced in rCsStefin-1-treated mice than DSS only-treated mice. In addition, the colon length of DSS only-treated mice was shorter than that of rCsStefin-1 treated mice. The secretion levels of IFN-γ and TNF-α in the spleen and mesenteric lymph nodes (MLNs) were significantly increased by DSS treatment, but the level of TNF-α in MLNs was significantly decreased by rCsStefin-1 treatment. IL-10 production in both spleen and MLNs was significantly increased, and IL-10⁺F4/80⁺ macrophage cells were significantly increased in the spleen and MLNs of rCsStefin-1 treated mice after DSS treatment. In conclusion, rCsStefin-1 could reduce the intestinal inflammation occurring after DSS treatment, these effects might be related with recruitment of IL-10 secreting macrophages.

Citations

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Identification and characterization of the second cysteine protease inhibitor of Clonorchis sinensis (CsStefin-2)
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Single Nucleotide Polymorphisms of Cytokine Genes are Associated with Fibrosis of the Intrahepatic Bile Duct Wall in Human Clonorchiasis: Byung-Suk Chung, Jeong-Keun Lee, Min-Ho Choi, Myoung Hee Park, Dongil Choi, Sung-Tae Hong; Korean J Parasitol 2009;47(2):145-151.
Published online May 27, 2009; DOI: https://doi.org/10.3347/kjp.2009.47.2.145

Abstract
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This study examined the association of cytokine gene polymorphisms with intrahepatic bile duct wall fibrosis in human clonorchiasis. A total of 240 residents in Heilongjiang, China underwent ultrasonography, blood sampling, and stool examination. Single nucleotide polymorphism (SNP) sites for IFN-γ (+874 T/A), IL-10 (-1,082 G/A, -819 C/T, -592 C/A), TNF-α (-308 G/A), and TGF-β1 (codon 10 T/C, codon 25 G/C) genes were observed with the TaqMan allelic discrimination assay. No significant correlation was observed between individual cytokine gene polymorphisms and intrahepatic duct dilatation (IHDD). Among individuals with clonorchiasis of moderate intensity, the incidence of IHDD was high in those with IFN-γ intermediate-producing genotype, +874AT (80.0%, P = 0.177), and in those with TNF-α low-producing genotype, -308GG (63.0%, P = 0.148). According to the combination of IFN-γ and TNF-α genotypes, the risks for IHDD could be stratified into high (intermediate-producing IFN-γ and low producing TNF-α), moderate, and low (low-producing IFN-γ and high producing TNF-α) risk groups. The incidence of IHDD was significantly different among these groups (P = 0.022): 88.9% (odds ratio, OR = 24.0) in high, 56.5% (OR = 3.9) in moderate, and 25.0% (OR = 1) in low risk groups. SNP of IFN-γ and TNF-α genes may contribute to the modulation of fibrosis in the intrahepatic bile duct wall in clonorchiasis patients.

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