<?xml version="1.0" encoding="UTF-8"?>
<feed xmlns="http://www.w3.org/2005/Atom" xmlns:dc="http://purl.org/dc/elements/1.1/">
  <title>DSpace Community:</title>
  <link rel="alternate" href="https://ir.ymlib.yonsei.ac.kr/handle/22282913/168790" />
  <subtitle />
  <id>https://ir.ymlib.yonsei.ac.kr/handle/22282913/168790</id>
  <updated>2026-04-07T23:21:45Z</updated>
  <dc:date>2026-04-07T23:21:45Z</dc:date>
  <entry>
    <title>Saccharomyces cerevisiae 48338 Suppresses Antibiotic-Induced Clostridioides difficile Infection in a Murine Model</title>
    <link rel="alternate" href="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211646" />
    <author>
      <name>Kim, Eunjung</name>
    </author>
    <author>
      <name>Kim, Hoyeon</name>
    </author>
    <author>
      <name>Lee, Minjae</name>
    </author>
    <author>
      <name>Kim, Beomjoong</name>
    </author>
    <author>
      <name>Kim, Bobae</name>
    </author>
    <author>
      <name>Kim, Haeun</name>
    </author>
    <author>
      <name>Kim, Dongyeol</name>
    </author>
    <author>
      <name>Kang, Dongjun</name>
    </author>
    <author>
      <name>Shatta, Arwa</name>
    </author>
    <author>
      <name>Kim, Ju Yeong</name>
    </author>
    <author>
      <name>Holzapfel, Wilhelm H.</name>
    </author>
    <author>
      <name>Yoon, Hongsup</name>
    </author>
    <id>https://ir.ymlib.yonsei.ac.kr/handle/22282913/211646</id>
    <updated>2026-03-31T01:29:49Z</updated>
    <published>2026-03-01T00:00:00Z</published>
    <summary type="text">Title: Saccharomyces cerevisiae 48338 Suppresses Antibiotic-Induced Clostridioides difficile Infection in a Murine Model
Authors: Kim, Eunjung; Kim, Hoyeon; Lee, Minjae; Kim, Beomjoong; Kim, Bobae; Kim, Haeun; Kim, Dongyeol; Kang, Dongjun; Shatta, Arwa; Kim, Ju Yeong; Holzapfel, Wilhelm H.; Yoon, Hongsup
Abstract: Clostridioides difficile infection (CDI) is a major cause of antibiotic-associated diarrhea and colitis, driven by toxin-mediated epithelial injury and inflammation. While antibiotics such as vancomycin remain the primary treatment, they can further disrupt the gut microbiota and promote recurrence. Probiotics, including yeast strains, have emerged as potential adjunctive therapies for mitigating CDI. In this study, several Saccharomyces cerevisiae strains were evaluated for their probiotic potential, and strain 48338 was identified as the most promising candidate based on its gastrointestinal tolerance, auto-aggregation ability, and antioxidant activity. Using a CDI mouse model, we found that treatment with S. cerevisiae 48338 reduced disease severity, as reflected by lower clinical sickness scores. Quantitative PCR analysis confirmed that the expression of the toxin gene tcdA was significantly decreased following 48338 treatment, whereas total C. difficile burden remained unchanged. In addition, 48338 treatment might enhance intestinal barrier integrity by upregulating occludin gene expression and also might attenuate production of pro-inflammatory cytokines, particularly the expression of IL-1 beta. The strain also increased the proportions of Foxp3+ regulatory T cells and macrophages in both the spleen and mesenteric lymph nodes, as determined by flow cytometry, suggesting a shift towards an anti-inflammatory immune profile. Collectively, these findings suggest that the primary mechanism by which S. cerevisiae 48338 exerts its protective effect against C. difficile infection is not through direct reduction of C. difficile colonization, but primarily through modulation of the microbiome, host immune response, and maintenance of epithelial cell integrity. This study highlights the potential of yeast-based probiotics as adjunctive agents for the prevention or mitigation of CDI.</summary>
    <dc:date>2026-03-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>IKK2, calcium, MAP kinase, and PI3 kinase are required for exocytosis and interleukin-8 production in human mast cells stimulated by Trichomonas vaginalis-derived secretory products</title>
    <link rel="alternate" href="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211695" />
    <author>
      <name>Park, Shin Hye</name>
    </author>
    <author>
      <name>Lee, Young Ah</name>
    </author>
    <author>
      <name>Shin, Myeong Heon</name>
    </author>
    <id>https://ir.ymlib.yonsei.ac.kr/handle/22282913/211695</id>
    <updated>2026-03-31T02:32:13Z</updated>
    <published>2026-01-01T00:00:00Z</published>
    <summary type="text">Title: IKK2, calcium, MAP kinase, and PI3 kinase are required for exocytosis and interleukin-8 production in human mast cells stimulated by Trichomonas vaginalis-derived secretory products
Authors: Park, Shin Hye; Lee, Young Ah; Shin, Myeong Heon
Abstract: Trichomonas vaginalis infection causes vaginitis and cervicitis in women, and asymptomatic urethritis and prostatitis in men. Mast cells play a key role in the inflammatory response against T. vaginalis infection. In this study, we examined the signaling pathways involved in mast cell activation induced by T. vaginalis-derived secretory products (TvSP), focusing on IKK2, calcium, MAP kinase (MAPK), and PI3 kinase (PI3K). TvSP stimulation induced phosphorylation and degradation of I kappa B, indicating NF-kappa B activation, and triggered phosphorylation of ERK1/2, p38 MAPK, and AKT. TvSP also increased the surface expression of CD63, a marker of exocytosis, which was reduced by IKK inhibition, calcium chelation, or blockade of PI3K and PKC. Furthermore, inhibition of PI3K or MAPKs decreased TvSP-induced interleukin-8 production. These results suggest that IKK2 and calcium are critical forTvSP-induced degranulation, while PI3K and MAPK pathways contribute to inter-leukin-8 production in mast cells.</summary>
    <dc:date>2026-01-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>3D enhancer architecture coordinated by CTCF determines immune-related gene expression patterns via RNA polymerase II pause-release in CD4+ T cells</title>
    <link rel="alternate" href="https://ir.ymlib.yonsei.ac.kr/handle/22282913/210194" />
    <author>
      <name>Lee, Eun-Chong</name>
    </author>
    <author>
      <name>Kim, Kyungwoo</name>
    </author>
    <author>
      <name>Kim, Sugyung</name>
    </author>
    <author>
      <name>Kim, Mikyoung</name>
    </author>
    <author>
      <name>Kim, Hyoung-Pyo</name>
    </author>
    <author>
      <name>이은총</name>
    </author>
    <id>https://ir.ymlib.yonsei.ac.kr/handle/22282913/210194</id>
    <updated>2026-01-22T05:18:50Z</updated>
    <published>2025-12-01T00:00:00Z</published>
    <summary type="text">Title: 3D enhancer architecture coordinated by CTCF determines immune-related gene expression patterns via RNA polymerase II pause-release in CD4+ T cells
Authors: Lee, Eun-Chong; Kim, Kyungwoo; Kim, Sugyung; Kim, Mikyoung; Kim, Hyoung-Pyo; 이은총
Abstract: CTCF (CCCTC-binding factor) is crucial for organizing mammalian genomes into domains and structural loops, yet its role in enhancer-promoter interactions remains unclear. Here, we demonstrate that 3D enhancer architecture undergoes marked reorganization upon CTCF depletion in activated CD4+ T cells. Despite this, active transcription, particularly driven by STAT5-bound super-enhancers, maintains enhancer loops independently of CTCF. Interestingly, robust enhancer-promoter interactions are associated with the release of RNA polymerase II (RNAPII) pausing and require CTCF-dependent 3D genome organization to shape immune-related gene expression patterns in CD4+ T cells. Notably, CTCF depletion reprograms the transcriptional response of CD4+ T cells to JAK inhibitors by rewiring the STAT5 enhancer network rather than altering the upstream JAK/STAT signaling cascade. This study emphasizes the role of 3D enhancer architecture orchestrated by CTCF and active transcription in directing precise cell identity gene expression through RNAPII pause-release in CD4+ T cells.</summary>
    <dc:date>2025-12-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Microbiome of Dipteran vectors associated with integron and antibiotic resistance genes in South Korea</title>
    <link rel="alternate" href="https://ir.ymlib.yonsei.ac.kr/handle/22282913/209206" />
    <author>
      <name>Chavarria, Xavier</name>
    </author>
    <author>
      <name>Shatta, Arwa</name>
    </author>
    <author>
      <name>Park, Hyun Seo</name>
    </author>
    <author>
      <name>Choi, Du-Yeol</name>
    </author>
    <author>
      <name>Kang, Dongjun</name>
    </author>
    <author>
      <name>Oh, Singeun</name>
    </author>
    <author>
      <name>Lee, Dawon</name>
    </author>
    <author>
      <name>Kim, Myungjun</name>
    </author>
    <author>
      <name>Choi, Jun Ho</name>
    </author>
    <author>
      <name>Cho, Yoon Hee</name>
    </author>
    <author>
      <name>Yi, Myung-hee</name>
    </author>
    <author>
      <name>Kim, Ju Yeong</name>
    </author>
    <id>https://ir.ymlib.yonsei.ac.kr/handle/22282913/209206</id>
    <updated>2026-01-19T02:12:31Z</updated>
    <published>2025-11-01T00:00:00Z</published>
    <summary type="text">Title: Microbiome of Dipteran vectors associated with integron and antibiotic resistance genes in South Korea
Authors: Chavarria, Xavier; Shatta, Arwa; Park, Hyun Seo; Choi, Du-Yeol; Kang, Dongjun; Oh, Singeun; Lee, Dawon; Kim, Myungjun; Choi, Jun Ho; Cho, Yoon Hee; Yi, Myung-hee; Kim, Ju Yeong
Abstract: The spread of antibiotic resistance genes (ARGs) across the environment and the role that organisms that interact with humans play as reservoirs of resistant bacteria pose important threats to public health. Flies are two-winged insects composing the order Diptera, which includes synanthropic species with significant ecological roles as pollinators, vectors, and decomposers. Here, we used iSeq100 metabarcoding to characterize the microbiome of six dipteran species in South Korea: Lucilia sericata, Lucilia illustris, Culex pipiens, Aedes vexans, Psychoda alternata and Clogmia albipunctata. We profiled a panel of common ARGs and performed correlation network analysis of the microbiome and resistome to identify co-occurrence patterns of bacterial amplicon sequence variants (ASVs) and resistance genes. We detected blaTEM, ermB, tetB, tetC, aac(6 &amp;apos;)-Ib-cr, cat2, sul1, qepA, int1 and int2, but no blaSHV, mecA, tetA or cat1. Notably, co-occurrence analysis showed highly mobile genes such as qepA, ermB and sul1 were associated with integron of class 1 integrase presence. These, along with aac(6 &amp;apos;)-Ib-cr were detected at higher rates across multiple species. Microbiome composition was distinct across species. Amplicon sequence variants (ASVs) of Pseudomonas, Corynebacterium, Clostridium, Ignatzschineria, Bacteroides, Streptococcus, Treponema and Dietzia showed strong co-occurrence with multiple ARGs. This study contributes to the understanding of the role of dipterans as reservoirs of antibiotic resistance.</summary>
    <dc:date>2025-11-01T00:00:00Z</dc:date>
  </entry>
</feed>

