Parasites, Hosts and Diseases

"Young Ah Lee"

Original Articles

Dynamin 2-mediated endocytosis of BLT1 is required for IL-8 production in HMC-1 cells induced by Trichomonas vaginalis-derived secretory products: Young Ah Lee, Myeong Heon Shin; Parasites Hosts Dis 2024;62(3):281-293.
Published online August 26, 2024; DOI: https://doi.org/10.3347/PHD.24049

We previously reported that leukotriene B₄ (LTB₄) contained in Trichomonas vaginalis-derived secretory products (TvSP) play an essential role in interleukin-8 (IL-8) production in human mast cell line (HMC-1 cells) via LTB₄ receptor (BLT)-mediated Nuclear Factor-kappa B (NF-_кB) activation. Dynamin, a GTPase, has been known to be involved in endocytosis of receptors for signaling of production of cytokine or chemokines. In the present study, we investigated the role of dynamin-mediated BLT1 endocytosis in TvSP-induced IL-8 production. When HMC-1 cells were transfected with BLT1 or BLT2 siRNA, TvSP-induced IL-8 production was significantly inhibited compared with that in cells transfected with control siRNA. In addition, pretreatment of HMC-1 cells with a dynamin inhibitor (Dynasore) reduced IL-8 production induced by TvSP or LTB₄. TvSP- or LTB₄- induced phosphorylation of NF-_кB was also attenuated by pretreatment with Dynasore. After exposing HMC-1 cells to TvSP or LTB₄, BLT1 was translocated from the intracellular compartments to the plasma membrane within 30 min. At 60 min after stimulation with TvSP or LTB₄, BLT1 remigrated from the cell surface to intracellular areas. Pretreatment of HMC-1 cells with dynamin-2 siRNA blocked internalization of BLT1 induced by TvSP or LTB₄. Co-immunoprecipitation experiments revealed that dynamin-2 strongly interacted with BLT1 60 min after stimulation with TvSP or LTB₄. These results suggest that T. vaginalis-secreted LTB₄ induces IL-8 production in HMC-1 cells via dynamin 2-mediated endocytosis of BLT1 and phosphorylation of NF-_кB.

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Detection of trichomonads in induced sputum from asthma patients in Korea
Myung-hee Yi, Myungjun Kim, Jun Ho Choi, Yoon Hee Cho, Hyun Kyung Oh, Jung-Won Park, Ju Yeong Kim
Parasites, Hosts and Diseases.2025; 63(3): 254. CrossRef

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CysLT receptor-mediated NOX2 activation is required for IL-8 production in HMC-1 cells induced by Trichomonas vaginalis-derived secretory products: Young Ah Lee, Myeong Heon Shin; Parasites Hosts Dis 2024;62(3):270-280.
Published online August 26, 2024; DOI: https://doi.org/10.3347/PHD.24046

Abstract
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Trichomoniasis is caused by a sexually transmitted flagellate protozoan parasite Trichomonas vaginalis. T. vaginalis-derived secretory products (TvSP) contain lipid mediators such as leukotriene B₄ (LTB₄) and various cysteinyl leukotrienes (CysLTs) which included LTC₄, LTD₄, and LTE₄. However, the signaling mechanisms by which T. vaginalis-induced CysLTs stimulate interleukin (IL)-8 production in human mast cells remain unclear. In this study, we investigated these mechanisms in human mast cells (HMC-1). Stimulation with TvSP resulted in increased intracellular reactive oxygen species (ROS) generation and NADPH oxidase 2 (NOX2) activation compared to unstimulated cells. Pre-treatment with NOX2 inhibitors such as diphenyleneiodonium chloride (DPI) or apocynin significantly reduced ROS production in TvSP-stimulated HMC-1 cells. Additionally, TvSP stimulation increased NOX2 protein expression and the translocation of p47^phox from the cytosol to the membrane. Pretreatment of HMC-1 cells with PI3K or PKC inhibitors reduced TvSP-induced p47^phox translocation and ROS generation. Furthermore, NOX2 inhibitors or NOX2 siRNA prevented CREB phosphorylation and IL-8 gene expression or protein secretion induced by TvSP. Pretreatment with a CysLTR antagonist significantly inhibited TvSP-induced ROS production, CREB phosphorylation, and IL-8 production. These results indicate that CysLT-mediated activation of NOX2 plays a crucial role in ROS-dependent IL-8 production in human mast cells stimulated by T. vaginalis-secreted CysLTs. These findings enhance our understanding of the inflammatory response in trichomoniasis and may inform the development of targeted therapies to mitigate this response.

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Untargeted metabolomics reveals postoperative metabolic dynamics in hepatic cystic echinococcosis patients
Kahaer Tuerxun, Abudouxikuer Abudoumijiti, Zainuer Yusupu, Rousitaimujiang Yimamu, Ronghua Tang, Ziru Wang, Abudoukeyimu Yasheng, Irshat Ibrahim, Yuanquan Wu
Immunobiology.2025; 230(4): 153099. CrossRef
Radical-induced lipid oxidation produces a torrent of leukotriene-like agonists in severe asthma
Si-Yang Liu, Mikhail Linetsky, Abby Hite, Yu-Shiuan Cheng, Masaru Miyagi, Serena C. Zhu, Hong Zeng, Siqi Huang, Myra Qin, Emma Sintic, Carolyn M. Koutures, Abigail Meneses, Olivia R. Laniak, Sailaja Paruchuri, Lakshminarayan R. Teegala, Kaixi Cui, Fariba
Journal of Allergy and Clinical Immunology.2025;[Epub] CrossRef

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Involvement of NOX2-derived ROS in human hepatoma HepG2 cell death induced by Entamoeba histolytica: Young Ah Lee, Myeong Heon Shin; Parasites Hosts Dis 2023;61(4):388-396.
Published online November 28, 2023; DOI: https://doi.org/10.3347/PHD.23094

Abstract
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Entamoeba histolytica is an enteric tissue-invasive protozoan parasite causing amoebic colitis and liver abscesses in humans. Amoebic contact with host cells activates intracellular signaling pathways that lead to host cell death via generation of caspase-3, calpain, Ca²⁺ elevation, and reactive oxygen species (ROS). We previously reported that various NADPH oxidases (NOXs) are responsible for ROS-dependent death of various host cells induced by amoeba. In the present study, we investigated the specific NOX isoform involved in ROS-dependent death of hepatocytes induced by amoebas. Co-incubation of hepatoma HepG2 cells with live amoebic trophozoites resulted in remarkably increased DNA fragmentation compared to cells incubated with medium alone. HepG2 cells that adhered to amoebic trophozoites showed strong dichlorodihydrofluorescein diacetate (DCF-DA) fluorescence, suggesting intracellular ROS accumulation within host cells stimulated by amoebic trophozoites. Pretreatment of HepG2 cells with the general NOX inhibitor DPI or NOX2-specific inhibitor GSK 2795039 reduced Entamoeba-induced ROS generation. Similarly, Entamoeba-induced LDH release from HepG2 cells was effectively inhibited by pretreatment with DPI or GSK 2795039. In NOX2-silenced HepG2 cells, Entamoeba-induced LDH release was also significantly inhibited compared with controls. Taken together, the results support an important role of NOX2-derived ROS in hepatocyte death induced by E. histolytica.

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CysLT receptor-mediated NOX2 activation is required for IL-8 production in HMC-1 cells induced by Trichomonas vaginalis-derived secretory products
Young Ah Lee, Myeong Heon Shin
Parasites, Hosts and Diseases.2024; 62(3): 270. CrossRef
Optimization of 18 S rRNA metabarcoding for the simultaneous diagnosis of intestinal parasites
Dongjun Kang, Jun Ho Choi, Myungjun Kim, Sohyeon Yun, Singeun Oh, Myung-hee Yi, Tai-Soon Yong, Young Ah Lee, Myeong Heon Shin, Ju Yeong Kim
Scientific Reports.2024;[Epub] CrossRef

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Mini Review

Signaling Role of NADPH Oxidases in ROS-Dependent Host Cell Death Induced by Pathogenic Entamoeba histolytica: Young Ah Lee, Seobo Sim, Kyeong Ah Kim, Myeong Heon Shin; Korean J Parasitol 2022;60(3):155-161.
Published online June 30, 2022; DOI: https://doi.org/10.3347/kjp.2022.60.3.155

Abstract
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All living organisms are destined to die. Cells, the core of those living creatures, move toward the irresistible direction of death. The question of how to die is critical and is very interesting. There are various types of death in life, including natural death, accidental death, questionable death, suicide, and homicide. The mechanisms and molecules involved in cell death also differ depending on the type of death. The dysenteric amoeba, E. histolytica, designated by the German zoologist Fritz Schaudinn in 1903, has the meaning of tissue lysis; i.e., tissue destroying, in its name. It was initially thought that the amoebae lyse tissue very quickly leading to cell death called necrosis. However, advances in measuring cell death have allowed us to more clearly investigate the various forms of cell death induced by amoeba. Increasing evidence has shown that E. histolytica can cause host cell death through induction of various intracellular signaling pathways. Understanding of the mechanisms and signaling molecules involved in host cell death induced by amoeba can provide new insights on the tissue pathology and parasitism in human amoebiasis. In this review, we emphasized on the signaling role of NADPH oxidases in reactive oxygen species (ROS)-dependent cell death by pathogenic E. histolytica.

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Involvement of NOX2-derived ROS in human hepatoma HepG2 cell death induced by Entamoeba histolytica
Young Ah Lee, Myeong Heon Shin
Parasites, Hosts and Diseases.2023; 61(4): 388. CrossRef

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Brief Communication

Naegleria fowleri Induces Jurkat T Cell Death via O-deGlcNAcylation: Young Ah Lee, Kyeong Ah Kim, Myeong Heon Shin; Korean J Parasitol 2021;59(5):501-505.
Published online October 22, 2021; DOI: https://doi.org/10.3347/kjp.2021.59.5.501

Abstract
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The pathogenic free-living amoeba Naegleria fowleri causes primary amoebic meningoencephalitis, a fatal infection, by penetrating the nasal mucosa and migrating to the brain via the olfactory nerves. N. fowleri can induce host cell death via lytic necrosis. Similar to phosphorylation, O-linked β-N-acetylglucosamine (O-GlcNAc) glycosylation (O-GlcNAcylation) is involved in various cell-signaling processes, including apoptosis and proliferation, with O-GlcNAc addition and removal regulated by O-GlcNAc transferase and O-GlcNAcase (OGA), respectively. However, the detailed mechanism of host cell death induced by N. fowleri is unknown. In this study, we investigated whether N. fowleri can induce the modulation of O-GlcNAcylated proteins during cell death in Jurkat T cells. Co-incubation with live N. fowleri trophozoites increased DNA fragmentation. In addition, incubation with N. fowleri induced a dramatic reduction in O-GlcNAcylated protein levels in 30 min. Moreover, pretreatment of Jurkat T cells with the OGA inhibitor PUGNAc prevented N. fowleri–induced O-deGlcNAcylation and DNA fragmentation. These results suggest that O-deGlcNAcylation is an important signaling process that occurs during Jurkat T cell death induced by N. fowleri.

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Primary amebic meningoencephalitis in children: A case report and literature review
Binbin Song, Junwen Zheng, Dongchi Zhao
IDCases.2024; 37: e02028. CrossRef

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Original Articles

Activation of MAPK Is Required for ROS Generation and Exocytosis in HMC-1 Cells Induced by Trichomonas vaginalis-Derived Secretory Products: Giimaa Narantsogt, Arim Min, Young Hee Nam, Young Ah Lee, Kyeong Ah Kim, Gurbadam Agvaandaram, Temuulen Dorjsuren, Jamel El-Benna, Myeong Heon Shin; Korean J Parasitol 2015;53(5):597-603.
Published online October 29, 2015; DOI: https://doi.org/10.3347/kjp.2015.53.5.597

Abstract
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Trichomonas vaginalis is a flagellated protozoan parasite that causes vaginitis and cervicitis in women and asymptomatic urethritis and prostatitis in men. Mast cells have been reported to be predominant in vaginal smears and vaginal walls of patients infected with T. vaginalis. Mitogen-activated protein kinase (MAPK), activated by various stimuli, have been shown to regulate the transcriptional activity of various cytokine genes in mast cells. In this study, we investigated whether MAPK is involved in ROS generation and exocytotic degranulation in HMC-1 cells induced by T. vaginalis-derived secretory products (TvSP). We found that TvSP induces the activation of MAPK and NADPH oxidase in HMC-1 cells. Stimulation with TvSP induced phosphorylation of MAPK and p47^phox in HMC-1 cells. Stimulation with TvSP also induced up-regulation of CD63, a marker for exocytosis, along the surfaces of human mast cells. Pretreatment with MAPK inhibitors strongly inhibited TvSP-induced ROS generation and exocytotic degranulation. Finally, our results suggest that TvSP induces intracellular ROS generation and exocytotic degranulation in HMC-1 via MAPK signaling.

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Dynamin 2-mediated endocytosis of BLT1 is required for IL-8 production in HMC-1 cells induced by Trichomonas vaginalis-derived secretory products
Young Ah Lee, Myeong Heon Shin
Parasites, Hosts and Diseases.2024; 62(3): 281. CrossRef
Trichomonas vaginalis excretory secretory proteins reduce semen quality and male fertility
Zhenchao Zhang, Fakun Li, Yangyang Deng, Yuhua Li, Wanxin Sheng, Xiaowei Tian, Zhenke Yang, Shuai Wang, Lihua Guo, Lixia Hao, Xuefang Mei
Acta Tropica.2023; 238: 106794. CrossRef
Latent Upregulation of Nlrp3, Nlrc4 and Aim2 Differentiates between Asymptomatic and Symptomatic Trichomonas vaginalis Infection
Sonal Yadav, Vivek Verma, Rakesh Singh Dhanda, Sumeeta Khurana, Manisha Yadav
Immunological Investigations.2022; 51(5): 1127. CrossRef
Trichomonas vaginalis Induces SiHa Cell Apoptosis by NF-κB Inactivation via Reactive Oxygen Species
Juan-Hua Quan, Byung-Hun Kang, Jung-Bo Yang, Yun-Ee Rhee, Heung-Tae Noh, In-Wook Choi, Guang-Ho Cha, Jae-Min Yuk, Young-Ha Lee
BioMed Research International.2017; 2017: 1. CrossRef
SNAP23-Dependent Surface Translocation of Leukotriene B 4 (LTB 4 ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secrete
Arim Min, Young Ah Lee, Kyeong Ah Kim, Jamel El-Benna, Myeong Heon Shin, Judith A. Appleton
Infection and Immunity.2017;[Epub] CrossRef
Explore the variation of MMP3, JNK, p38 MAPKs, and autophagy at the early stage of osteoarthritis
Jie Shi, Changjie Zhang, Zhongjie Yi, Chunna Lan
IUBMB Life.2016; 68(4): 293. CrossRef

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Degradation of the Transcription Factors NF-κB, STAT3, and STAT5 Is Involved in Entamoeba histolytica-Induced Cell Death in Caco-2 Colonic Epithelial Cells: Kyeong Ah Kim, Arim Min, Young Ah Lee, Myeong Heon Shin; Korean J Parasitol 2014;52(5):459-469.
Published online October 22, 2014; DOI: https://doi.org/10.3347/kjp.2014.52.5.459

Abstract
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Entamoeba histolytica is a tissue-invasive protozoan parasite causing dysentery in humans. During infection of colonic tissues, amoebic trophozoites are able to kill host cells via apoptosis or necrosis, both of which trigger IL-8-mediated acute inflammatory responses. However, the signaling pathways involved in host cell death induced by E. histolytica have not yet been fully defined. In this study, we examined whether calpain plays a role in the cleavage of pro-survival transcription factors during cell death of colonic epithelial cells, induced by live E. histolytica trophozoites. Incubation with amoebic trophozoites induced activation of m-calpain in a time- and dose-dependent manner. Moreover, incubation with amoebae resulted in marked degradation of STAT proteins (STAT3 and STAT5) and NF-κB (p65) in Caco-2 cells. However, IκB, an inhibitor of NF-κB, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-κB was partially inhibited by pretreatment of cells with a cell-permeable calpain inhibitor, calpeptin. In contrast, E. histolytica did not induce cleavage of caspase-3 in Caco-2 cells. Furthermore, pretreatment of Caco-2 cells with a calpain inhibitor, calpeptin (but not the pan-caspase inhibitor, z-VAD-fmk) or m-calpain siRNA partially reduced Entamoeba-induced DNA fragmentation in Caco-2 cells. These results suggest that calpain plays an important role in E. histolytica-induced degradation of NF-κB and STATs in colonic epithelial cells, which ultimately accelerates cell death.

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Proteomics on choroidal neovascularization based on itraq and the protective effect of TAB1 in CNV
Yong Du, Shaoqiu Jiang, Lujia Feng, Jing Lu, Hui Peng, Xiyuan Zhou
Scientific Reports.2025;[Epub] CrossRef
CAPN5 attenuates cigarette smoke extract-induced apoptosis and inflammation in BEAS-2B cells
Herui Li, Yiming Ma, Tiao Li, Zihang Zeng, Lijuan Luo, Xiangming Liu, Yi Li, Yan Chen
Tobacco Induced Diseases.2024; 22(April): 1. CrossRef
miR-146a-5p promotes epithelium regeneration against LPS-induced inflammatory injury via targeting TAB1/TAK1/NF-κB signaling pathway
Xingping Chen, Weite Li, Ting Chen, Xiaohui Ren, Jiahao Zhu, Fangxin Hu, Junyi Luo, Lipeng Xing, Hao Zhou, Jiajie Sun, Qingyan Jiang, Yongliang Zhang, Qianyun Xi
International Journal of Biological Macromolecules.2022; 221: 1031. CrossRef
The NF-κB Pathway: Modulation by Entamoeba histolytica and Other Protozoan Parasites
Attinder Chadha, Kris Chadee
Frontiers in Cellular and Infection Microbiology.2021;[Epub] CrossRef
Entamoeba histolytica activation of caspase-1 degrades cullin that attenuates NF-κB dependent signaling from macrophages
Attinder Chadha, France Moreau, Shanshan Wang, Antoine Dufour, Kris Chadee, Dario S. Zamboni
PLOS Pathogens.2021; 17(9): e1009936. CrossRef
Entamoeba histolytica Up-Regulates MicroRNA-643 to Promote Apoptosis by Targeting XIAP in Human Epithelial Colon Cells
Itzel López-Rosas, César López-Camarillo, Yarely M. Salinas-Vera, Olga N. Hernández-de la Cruz, Carlos Palma-Flores, Bibiana Chávez-Munguía, Osbaldo Resendis-Antonio, Nancy Guillen, Carlos Pérez-Plasencia, María Elizbeth Álvarez-Sánchez, Esther Ramírez-Mo
Frontiers in Cellular and Infection Microbiology.2019;[Epub] CrossRef
Gene Profile Expression Related to Type I Interferons in HT-29 Cells Exposed to Cryptosporidium parvum
Seyede Manizhe Heidarnejadi, Abdollah Rafiei, Manoochehr Makvandi, Majid Pirestani, Jasem Saki, Ataallah Ghadiri
Jundishapur Journal of Microbiology.2018;[Epub] CrossRef
O-deGlcNAcylation is required for Entamoeba histolytica-induced HepG2 cell death
Young Ah Lee, Arim Min, Myeong Heon Shin
Microbial Pathogenesis.2018; 123: 285. CrossRef
Infection Strategies of Intestinal Parasite Pathogens and Host Cell Responses
Bruno M. Di Genova, Renata R. Tonelli
Frontiers in Microbiology.2016;[Epub] CrossRef

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Amoebic PI3K and PKC Is Required for Jurkat T Cell Death Induced by Entamoeba histolytica: Young Ah Lee, Kyeong Ah Kim, Arim Min, Myeong Heon Shin; Korean J Parasitol 2014;52(4):355-365.
Published online August 29, 2014; DOI: https://doi.org/10.3347/kjp.2014.52.4.355

Abstract
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The enteric protozoan parasite Entamoeba histolytica is the causative agent of human amebiasis. During infection, adherence of E. histolytica through Gal/GalNAc lectin on the surface of the amoeba can induce caspase-3-dependent or -independent host cell death. Phosphorylinositol 3-kinase (PI3K) and protein kinase C (PKC) in E. histolytica play an important function in the adhesion, killing, or phagocytosis of target cells. In this study, we examined the role of amoebic PI3K and PKC in amoeba-induced apoptotic cell death in Jurkat T cells. When Jurkat T cells were incubated with E. histolytica trophozoites, phosphatidylserine (PS) externalization and DNA fragmentation in Jurkat cells were markedly increased compared to those of cells incubated with medium alone. However, when amoebae were pretreated with a PI3K inhibitor, wortmannin before being incubated with E. histolytica, E. histolytica-induced PS externalization and DNA fragmentation in Jurkat cells were significantly reduced compared to results for amoebae pretreated with DMSO. In addition, pretreatment of amoebae with a PKC inhibitor, staurosporine strongly inhibited Jurkat T cell death. However, E. histolytica-induced cleavage of caspase-3, -6, and -7 were not inhibited by pretreatment of amoebae with wortmannin or staurosporin. In addition, we found that amoebic PI3K and PKC have an important role on amoeba adhesion to host compartment. These results suggest that amebic PI3K and PKC activation may play an important role in caspase-independent cell death in Entamoeba-induced apoptosis.

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Lujun Yan, Yating Li, Xing Yang, Rui Li, Chunyin Zhu, Xuedong He, Xiaoliang Jin, Guanghui Zheng, Naunain Mehmood, William C. Cho, Shijun Bao, Houhui Song, Yadong Zheng
Virulence.2025;[Epub] CrossRef
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Shijiao Li, Jingjiang Qiu, Zhongwei Guo, Qiulei Gao, Chen-Yu Huang, Yilin Hao, Yifan Hu, Tianshui Liang, Ming Zhai, Yudong Zhang, Bangbang Nie, Wei-Jen Chang, Wen Wang, Rui Xi, Ronghan Wei
Biofabrication.2024; 16(4): 045018. CrossRef
AGC family kinase of Entamoeba histolytica: Decoding the members biochemically
Azhar Ahmad, Vikas Kumar, Tushar Kushwaha, Akash Kumar, Deepak Sehgal, Krishna K. Inampudi, Somlata, Katherine S. Ralston
PLOS Pathogens.2024; 20(11): e1012729. CrossRef
Pathogenicity and virulence of Entamoeba histolytica , the agent of amoebiasis
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Virulence.2023;[Epub] CrossRef
Apoptotic mimicry as a strategy for the establishment of parasitic infections: parasite- and host-derived phosphatidylserine as key molecule
João Luiz Mendes Wanderley, Renato Augusto DaMatta, Marcello André Barcinski
Cell Communication and Signaling.2020;[Epub] CrossRef
Entamoeba histolytica Up-Regulates MicroRNA-643 to Promote Apoptosis by Targeting XIAP in Human Epithelial Colon Cells
Itzel López-Rosas, César López-Camarillo, Yarely M. Salinas-Vera, Olga N. Hernández-de la Cruz, Carlos Palma-Flores, Bibiana Chávez-Munguía, Osbaldo Resendis-Antonio, Nancy Guillen, Carlos Pérez-Plasencia, María Elizbeth Álvarez-Sánchez, Esther Ramírez-Mo
Frontiers in Cellular and Infection Microbiology.2019;[Epub] CrossRef
Phosphatidylinositol Kinases and Phosphatases in Entamoeba histolytica
Kumiko Nakada-Tsukui, Natsuki Watanabe, Tomohiko Maehama, Tomoyoshi Nozaki
Frontiers in Cellular and Infection Microbiology.2019;[Epub] CrossRef
AGC family kinase 1 participates in trogocytosis but not in phagocytosis in Entamoeba histolytica
Somlata, Kumiko Nakada-Tsukui, Tomoyoshi Nozaki
Nature Communications.2017;[Epub] CrossRef

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Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS: Kyeong Ah Kim, Ju Young Kim, Young Ah Lee, Arim Min, Young Yil Bahk, Myeong Heon Shin; Korean J Parasitol 2013;51(1):61-68.
Published online February 18, 2013; DOI: https://doi.org/10.3347/kjp.2013.51.1.61

Abstract
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Entamoeba histolytica, which causes amoebic colitis and occasionally liver abscess in humans, is able to induce host cell death. However, signaling mechanisms of colon cell death induced by E. histolytica are not fully elucidated. In this study, we investigated the signaling role of NOX in cell death of HT29 colonic epithelial cells induced by E. histolytica. Incubation of HT29 cells with amoebic trophozoites resulted in DNA fragmentation that is a hallmark of apoptotic cell death. In addition, E. histolytica generate intracellular reactive oxygen species (ROS) in a contact-dependent manner. Inhibition of intracellular ROS level with treatment with DPI, an inhibitor of NADPH oxidases (NOXs), decreased Entamoeba-induced ROS generation and cell death in HT29 cells. However, pan-caspase inhibitor did not affect E. histolytica-induced HT29 cell death. In HT29 cells, catalytic subunit NOX1 and regulatory subunit Rac1 for NOX1 activation were highly expressed. We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Suppression of Rac1 by siRNA significantly inhibited Entamoeba-induced cell death. Moreover, knockdown of NOX1 by siRNA, effectively inhibited E. histolytica-triggered DNA fragmentation in HT29 cells. These results suggest that NOX1-derived ROS is required for apoptotic cell death in HT29 colon epithelial cells induced by E. histolytica.

Citations

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Involvement of NOX2-derived ROS in human hepatoma HepG2 cell death induced by Entamoeba histolytica
Young Ah Lee, Myeong Heon Shin
Parasites, Hosts and Diseases.2023; 61(4): 388. CrossRef
Signaling Role of NADPH Oxidases in ROS-Dependent Host Cell Death Induced by Pathogenic Entamoeba histolytica
Young Ah Lee, Seobo Sim, Kyeong Ah Kim, Myeong Heon Shin
The Korean Journal of Parasitology.2022; 60(3): 155. CrossRef
The interaction betweenEntamoeba histolyticaand enterobacteria shed light on an ancient antibacterial response
Nancy Guillén
Cellular Microbiology.2019;[Epub] CrossRef
NOX4 activation is involved in ROS‐dependent Jurkat T‐cell death induced by Entamoeba histolytica
Young Ah Lee, Kyeong Ah Kim, Arim Min, Myeong Heon Shin
Parasite Immunology.2019;[Epub] CrossRef
O-deGlcNAcylation is required for Entamoeba histolytica-induced HepG2 cell death
Young Ah Lee, Arim Min, Myeong Heon Shin
Microbial Pathogenesis.2018; 123: 285. CrossRef
GOLPH3 expression promotes the resistance of HT29 cells to 5‑fluorouracil by activating multiple signaling pathways
Ming‑Zhen Wang, Cheng‑Zhi Qiu, Wai‑Shi Yu, Yan‑Ta Guo, Chun‑Xiao Wang, Zhi‑Xiong Chen
Molecular Medicine Reports.2017;[Epub] CrossRef
Infection Strategies of Intestinal Parasite Pathogens and Host Cell Responses
Bruno M. Di Genova, Renata R. Tonelli
Frontiers in Microbiology.2016;[Epub] CrossRef
A whole-genome RNAi screen uncovers a novel role for human potassium channels in cell killing by the parasite Entamoeba histolytica
Chelsea Marie, Hans P. Verkerke, Dan Theodorescu, William A. Petri
Scientific Reports.2015;[Epub] CrossRef
Degradation of the Transcription Factors NF-κB, STAT3, and STAT5 Is Involved in Entamoeba histolytica-Induced Cell Death in Caco-2 Colonic Epithelial Cells
Kyeong Ah Kim, Arim Min, Young Ah Lee, Myeong Heon Shin
The Korean Journal of Parasitology.2014; 52(5): 459. CrossRef
Protective action of NADPH oxidase inhibitors and role of NADPH oxidase in pathogenesis of colon inflammation in mice
Rima Ramonaite
World Journal of Gastroenterology.2014; 20(35): 12533. CrossRef
Small GTPases of the Ras superfamily regulate intestinal epithelial homeostasis and barrier function via common and unique mechanisms
Alí Francisco Citalán-Madrid, Alexander García-Ponce, Hilda Vargas-Robles, Abigail Betanzos, Michael Schnoor
Tissue Barriers.2013; 1(5): e26938. CrossRef
The EhCPADH112 Complex of Entamoeba histolytica Interacts with Tight Junction Proteins Occludin and Claudin-1 to Produce Epithelial Damage
Abigail Betanzos, Rosario Javier-Reyna, Guillermina García-Rivera, Cecilia Bañuelos, Lorenza González-Mariscal, Michael Schnoor, Esther Orozco, Johanna M. Brandner
PLoS ONE.2013; 8(6): e65100. CrossRef

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Brief Communications

NF-κB and CREB Are Involved in IL-8 Production of Human Neutrophils Induced by Trichomonas vaginalis-Derived Secretory Products: Young Hee Nam, Deulle Min, Soon-Jung Park, Kyeong Ah Kim, Young Ah Lee, Myeong Heon Shin; Korean J Parasitol 2011;49(3):291-294.
Published online September 30, 2011; DOI: https://doi.org/10.3347/kjp.2011.49.3.291

Abstract
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Trichomonas vaginalis is a flagellated lumen-dwelling extracellular protozoan parasite that causes human trichomoniasis via sexual intercourse. Human neutrophils play a crucial role in acute tissue inflammatory responses in T. vaginalis infection. In this study, we investigated the signaling mechanism of neutrophil responses when stimulated with T. vaginalis-derived secretory products (TvSP), which were collected from 1×10⁷ live trichomonads. Incubation of human neutrophils isolated from peripheral blood with TvSP induced up-regulation of IL-8 protein secretion. In addition, stimulation with TvSP induced phosphorylation of NF-κB and CREB in neutrophils. Moreover, TvSP-induced IL-8 production was also significantly inhibited by pretreatment of neutrophils with iκB inhibitor or CREB inhibitor. These results suggest that transcription factors NF-κB and CREB are involved in IL-8 production in human neutrophils induced by stimulation with T. vaginalis infection.

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Trichomonas vaginalis extracellular vesicles suppress IFNε-mediated responses driven by its intracellular bacterial symbiont Mycoplasma hominis
Joshua A. Kochanowsky, Emma L. Betts, Gabriel Encinas, Johnson Amoah, Patricia J. Johnson
Proceedings of the National Academy of Sciences.2025;[Epub] CrossRef
CysLT receptor-mediated NOX2 activation is required for IL-8 production in HMC-1 cells induced by Trichomonas vaginalis-derived secretory products
Young Ah Lee, Myeong Heon Shin
Parasites, Hosts and Diseases.2024; 62(3): 270. CrossRef
Trichomonas vaginalis excretory secretory proteins reduce semen quality and male fertility
Zhenchao Zhang, Fakun Li, Yangyang Deng, Yuhua Li, Wanxin Sheng, Xiaowei Tian, Zhenke Yang, Shuai Wang, Lihua Guo, Lixia Hao, Xuefang Mei
Acta Tropica.2023; 238: 106794. CrossRef
Increased Angiogenesis by Exosomes Secreted by Adipose-Derived Stem Cells upon Lipopolysaccharide Stimulation
Shao-Chun Wu, Pao-Jen Kuo, Cheng-Shyuan Rau, Lien-Hung Huang, Chia-Wei Lin, Yi-Chan Wu, Chia-Jung Wu, Chia-Wen Tsai, Ting-Min Hsieh, Hang-Tsung Liu, Chun-Ying Huang, Ching-Hua Hsieh
International Journal of Molecular Sciences.2021; 22(16): 8877. CrossRef
Trichomonas vaginalis‐secreted cysteinyl leukotrienes promote migration, degranulation and MCP‐1 production in mast cells
Young Ah Lee, Young Hee Nam, Arim Min, Myeong Heon Shin
Parasite Immunology.2020;[Epub] CrossRef
PKA/CREB and NF-κB pathway regulates AKNA transcription: A novel insight into T-2 toxin-induced inflammation and GH deficiency in GH3 cells
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SNAP23-Dependent Surface Translocation of Leukotriene B 4 (LTB 4 ) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secrete
Arim Min, Young Ah Lee, Kyeong Ah Kim, Jamel El-Benna, Myeong Heon Shin, Judith A. Appleton
Infection and Immunity.2017;[Epub] CrossRef
Influence of functional polymorphisms in TNF-α, IL-8, and IL-10 cytokine genes on mRNA expression levels and risk of gastric cancer
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The Pathogenesis of Human Cervical Epithelium Cells Induced by Interacting with Trichomonas vaginalis
Wei-Chen Lin, Wei-Ting Chang, Tsuey-Yu Chang, Jyh-Wei Shin, Xuefeng Liu
PLOS ONE.2015; 10(4): e0124087. CrossRef

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Calpains are Involved in Entamoeba histolytica-Induced Death of HT-29 Colonic Epithelial Cells: Yun Soo Jang, Kyoung-Ju Song, Ju Young Kim, Young Ah Lee, Kyeong Ah Kim, Sang Kyou Lee, Myeong Heon Shin; Korean J Parasitol 2011;49(2):177-180.
Published online June 14, 2011; DOI: https://doi.org/10.3347/kjp.2011.49.2.177

Abstract
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Entamoeba histolytica is an enteric tissue-invading protozoan parasite that can cause amebic colitis and liver abscess in humans. E. histolytica has the capability to kill colon epithelial cells in vitro; however, information regarding the role of calpain in colon cell death induced by ameba is limited. In this study, we investigated whether calpains are involved in the E. histolytica-induced cell death of HT-29 colonic epithelial cells. When HT-29 cells were co-incubated with E. histolytica, the propidium iodide stained dead cells markedly increased compared to that in HT-29 cells incubated with medium alone. This pro-death effect induced by ameba was effectively blocked by pretreatment of HT-29 cells with the calpain inhibitor, calpeptin. Moreover, knockdown of m- and ?-calpain by siRNA significantly reduced E. histolytica-induced HT-29 cell death. These results suggest that m- and ?-calpain may be involved in colon epithelial cell death induced by E. histolytica.

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Involvement of NOX2-derived ROS in human hepatoma HepG2 cell death induced by Entamoeba histolytica
Young Ah Lee, Myeong Heon Shin
Parasites, Hosts and Diseases.2023; 61(4): 388. CrossRef
Signaling Role of NADPH Oxidases in ROS-Dependent Host Cell Death Induced by Pathogenic Entamoeba histolytica
Young Ah Lee, Seobo Sim, Kyeong Ah Kim, Myeong Heon Shin
The Korean Journal of Parasitology.2022; 60(3): 155. CrossRef
Infection Strategies of Intestinal Parasite Pathogens and Host Cell Responses
Bruno M. Di Genova, Renata R. Tonelli
Frontiers in Microbiology.2016;[Epub] CrossRef
Degradation of the Transcription Factors NF-κB, STAT3, and STAT5 Is Involved in Entamoeba histolytica-Induced Cell Death in Caco-2 Colonic Epithelial Cells
Kyeong Ah Kim, Arim Min, Young Ah Lee, Myeong Heon Shin
The Korean Journal of Parasitology.2014; 52(5): 459. CrossRef
Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS
Kyeong Ah Kim, Ju Young Kim, Young Ah Lee, Arim Min, Young Yil Bahk, Myeong Heon Shin
The Korean Journal of Parasitology.2013; 51(1): 61. CrossRef
Mechanisms of Adherence, Cytotoxicity and Phagocytosis Modulate the Pathogenesis of Entamoeba Histolytica
Nathaniel CV Christy, William A Petri
Future Microbiology.2011; 6(12): 1501. CrossRef

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Original Article

Involvement of Src Family Tyrosine Kinase in Apoptosis of Human Neutrophils Induced by Protozoan Parasite Entamoeba histolytica: Seobo Sim, Jae-Ran Yu, Young Ah Lee, Myeong Heon Shin; Korean J Parasitol 2010;48(4):285-290.
Published online December 16, 2010; DOI: https://doi.org/10.3347/kjp.2010.48.4.285

Abstract
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Tyrosine kinases are one of the most important regulators for intracellular signal transduction related to inflammatory responses. However, there are no reports describing the effects of tyrosine kinases on neutrophil apoptosis induced by Entamoeba histolytica. In this study, isolated human neutrophils from peripheral blood were incubated with live trophozoites in the presence or absence of tyrosine kinase inhibitors. Entamoeba-induced receptor shedding of CD16 and PS externalization in neutrophils were inhibited by pre-incubation of neutrophils with the broad-spectrum tyrosine kinase inhibitor genistein or the Src family kinase inhibitor PP2. Entamoeba-induced ROS production was also inhibited by genistein or PP2. Moreover, genistein and PP2 blocked the phosphorylation of ERK and p38 MAPK in neutrophils induced by E. histolytica. These results suggest that Src tyrosine kinases may participate in the signaling event for ROS-dependent activation of MAPKs during neutrophil apoptosis induced by E. histolytica.

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Differential expression of ADAM15 and ADAM17 metalloproteases in the rat brain after severe hypobaric hypoxia and hypoxic preconditioning
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Neuroscience Research.2012; 72(4): 364. CrossRef

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Mini Review

Eosinophil-Mediated Tissue Inflammatory Responses in Helminth Infection: Myeong Heon Shin, Young Ah Lee, Duk-Young Min; Korean J Parasitol 2009;47(Suppl):S125.
Published online October 26, 2009; DOI: https://doi.org/10.3347/kjp.2009.47.S.S125

Abstract
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Eosinophilic leukocytes function in host protection against parasitic worms. In turn, helminthic parasites harbor specific molecules to evade or paralyze eosinophil-associated host immune responses; these molecules facilitate the migration and survival of parasitic helminths in vivo. This competition between eosinophil and worm leads to stable equilibria between them. An understanding of such dynamic host-eosinophil interactions will help us to uncover mechanisms of cross talk between host and parasite in helminth infection. In this review, we examine recent findings regarding the innate immune responses of eosinophils to helminthic parasites, and discuss the implications of these findings in terms of eosinophil-mediated tissue inflammation in helminth infection.

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