Journal of Microbiology

Eun Hee Jeong

1 Article

A Comparison of Adult and Pediatric Methicillin-Resistant Staphylococcus aureus Isolates Collected from Patients at a University Hospital in Korea: Jin Yeol Park , Jong Sook Jin , Hee Young Kang , Eun Hee Jeong , Je Chul Lee , Yoo Chul Lee , Sung Yong Seol , Dong Taek Cho , Jungmin Kim; J. Microbiol. 2007;45(5):447-452.; DOI: https://doi.org/2591 [pii]

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Abstract PDF: In this study, we compared the phenotypic and genotypic characteristics of 138 MRSA isolates obtained from adult and pediatric patients (adult, 50; children, 88). The resistance rates against gentamicin, clindamycin, and ciprofloxacin were much higher in the adult MRSA isolates than in the pediatric MRSA isolates. The ermC gene, which is responsible for inducible clindamycin resistance, was detected in 52(59.1%) of the 88 pediatric MRSA isolates but in only 5(10.0%) of the 50 adult MRSA isolates. MRSA isolates of clonal type ST5 with an integration of SCCmec type II/II variants was the most predominant clone among the adult isolates, while clonal type ST72 with an integration of SCCmec IV/IVA was the most predominant clone among the pediatric MRSA isolates. Staphylococcal enterotoxin A and toxic shock syndrome toxin-1 were prevalent among the adult MRSA isolates but not among the pediatric MRSA isolates. The results of this study demonstrated remarkable differences between adult and pediatric MRSA isolates in terms of their antimicrobial susceptibility profiles, SCCmec type, multilocus sequence type, staphylococcal toxin genes, and erythromycin resistance genes.

Eun Hee Jeong

2 Articles

Development of tri-cistronic CLDN18.2 CAR-T cells incorporating PD-1/CD28 switch and cyclophilin A for enhanced solid tumor immunotherapy: Heon Ju Lee, Seo Jin Hwang, Eun Hee Jeong, Mi Hee Chang, Bu Yeon Heo, Jaeyul Kwon, Yoona Noh, Jihoon Nah; J. Microbiol. 2026;64(1):e2510017. Published online January 31, 2026; DOI: https://doi.org/10.71150/jm.2510017

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Abstract PDF Supplementary Material: Chimeric antigen receptor (CAR)-T cell therapy holds significant potential for the treatment of solid tumors. However, immune suppression and tumor-specific barriers limit its application. Claudin 18.2 (CLDN18.2), a gastric lineage-specific tight junction protein highly expressed in gastric and pancreatic cancers, is a promising therapeutic target. In this study, we aimed to develop a next-generation tri-cistronic CLDN18.2-directed CAR-T cell platform that integrates a programmed cell death protein 1 (PD-1)/CD28 chimeric switch receptor with cyclophilin A (CypA). This platform sought to counteract PD-1–mediated immunosuppression and enhance T-cell activation and persistence. We generated CLDN18.2 CAR-T cells incorporating costimulatory inducible T-cell costimulator (ICOS) domains using lentiviral vector-based recombinant engineering. We further evaluated their cytokine release, cytotoxic activity, and safety profiles. In vitro, tri-cistronic CAR-T cells exhibited markedly increased interferon γ and tumor necrosis factor α secretion and enhanced cytotoxicity against CLDN18.2-positive gastric cancer cells compared with conventional CAR-T constructs. In vivo, these cells showed superior antitumor efficacy and sustained tumor regression without observable toxicity in xenograft gastric cancer models. Collectively, these findings demonstrate that the integration of PD-1/CD28 signaling and CypA within a tri-cistronic framework significantly reinforces CAR-T cell functionality and durability. This suggests strong clinical potential as a next-generation immunotherapy for solid tumors.

Genetically Engineered CLDN18.2 CAR-T Cells Expressing Synthetic PD1/CD28 Fusion Receptors Produced Using a Lentiviral Vector: Heon Ju Lee, Seo Jin Hwang, Eun Hee Jeong, Mi Hee Chang; J. Microbiol. 2024;62(7):555-568. Published online May 3, 2024; DOI: https://doi.org/10.1007/s12275-024-00133-0

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Abstract PDF

This study aimed to develop synthetic Claudin18.2 (CLDN18.2) chimeric antigen receptor (CAR)-T (CAR-T) cells as a treatment for advanced gastric cancer using lentiviral vector genetic engineering technology that targets the CLDN18.2 antigen and simultaneously overcomes the immunosuppressive environment caused by programmed cell death protein 1 (PD-1). Synthetic CAR T cells are a promising approach in cancer immunotherapy but face many challenges in solid tumors. One of the major problems is immunosuppression caused by PD-1. CLDN18.2, a gastric-specific membrane protein, is considered a potential therapeutic target for gastric and other cancers. In our study, CLDN18.2 CAR was a second-generation CAR with inducible T-cell costimulatory (CD278), and CLDN18.2-PD1/CD28 CAR was a third-generation CAR, wherein the synthetic PD1/CD28 chimeric-switch receptor (CSR) was added to the second-generation CAR. In vitro, we detected the secretion levels of different cytokines and the killing ability of CAR-T cells. We found that the secretion of cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) secreted by three types of CAR-T cells was increased, and the killing ability against CLDN18.2-positive GC cells was enhanced. In vivo, we established a xenograft GC model and observed the antitumor effects and off-target toxicity of CAR-T cells. These results support that synthetic anti-CLDN18.2 CAR-T cells have antitumor effect and anti-CLDN18.2-PD1/CD28 CAR could provide a promising design strategy to improve the efficacy of CAR-T cells in advanced gastric cancer.

Citations

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Tumor microenvironment in gastric cancer immune tolerance and its therapeutic relevance in immunomodulation (Review)
Zihe Guan, Lichao Han, Baojiang Chen, Yijia Ma, Qianyue Ni, Zijian Wang, Jingyu Yang, Zheng Liu
Oncology Letters.2026;[Epub] CrossRef
Development of tri-cistronic CLDN18.2 CAR-T cells incorporating PD-1/CD28 switch and cyclophilin A for enhanced solid tumor immunotherapy
Heon Ju Lee, Seo Jin Hwang, Eun Hee Jeong, Mi Hee Chang, Bu Yeon Heo, Jaeyul Kwon, Yoona Noh, Jihoon Nah
Journal of Microbiology.2026; 64(1): e2510017. CrossRef
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Nature Communications.2025;[Epub] CrossRef
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Biomedicine & Pharmacotherapy.2025; 193: 118863. CrossRef
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Molecular Cancer.2025;[Epub] CrossRef

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