Yun‐Gi Kim

ORCID: 0000-0003-4251-1848
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About
Contact & Profiles
Research Areas
  • Gut microbiota and health
  • Immune Response and Inflammation
  • Clostridium difficile and Clostridium perfringens research
  • Inflammasome and immune disorders
  • Immune Cell Function and Interaction
  • Plasma Diagnostics and Applications
  • Vibrio bacteria research studies
  • Immune cells in cancer
  • Escherichia coli research studies
  • Mercury impact and mitigation studies
  • Vector-borne infectious diseases
  • TiO2 Photocatalysis and Solar Cells
  • Diet and metabolism studies
  • Diet, Metabolism, and Disease
  • Pediatric health and respiratory diseases
  • Probiotics and Fermented Foods
  • COVID-19 Clinical Research Studies
  • Liver Disease Diagnosis and Treatment
  • Neonatal Respiratory Health Research
  • Pancreatic and Hepatic Oncology Research
  • Advancements in Semiconductor Devices and Circuit Design
  • Advanced Photocatalysis Techniques
  • Semiconductor materials and devices
  • Phagocytosis and Immune Regulation
  • Nosocomial Infections in ICU

Kitasato University
2003-2025

Keio University
2016-2024

Vedantra Pharmaceuticals (United States)
2022

University of Michigan
2007-2017

Jeju National University
2014-2016

University of Tsukuba
2014

Japan Science and Technology Agency
2014

Pusan National University
2010-2012

Dankook University
2012

Seoul National University Hospital
2012

The virulence mechanisms that allow pathogens to colonize the intestine remain unclear. Here, we show germ-free animals are unable eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria. Early in infection, genes were expressed required pathogen growth conventionally raised mice but not mice. Virulence gene expression was down-regulated during late phase of which led relocation intestinal lumen where it outcompeted by commensals. ability commensals...

10.1126/science.1222195 article EN Science 2012-05-11

Abstract RICK is a kinase that has been implicated in Nod1 and Nod2 signaling. In addition, proposed to mediate TLR signaling its absence confers reduced responses certain bacterial products such as LPS. We show here macrophages mice lacking are defective their agonists but exhibit unimpaired synthetic highly purified agonists. Furthermore, production of chemokines induced by the dipeptide γ-d-glutamyl-meso-diaminopimelic acid was intact MyD88 deficient abolished RICK-null mice. Stimulation...

10.4049/jimmunol.178.4.2380 article EN The Journal of Immunology 2007-02-15

The high susceptibility of neonates to infections has been assumed be due immaturity the immune system, but mechanism remains unclear. By colonizing adult germ-free mice with cecal contents neonatal and mice, we show that microbiota is unable prevent colonization by two bacterial pathogens cause mortality in neonates. lack resistance occurred when Clostridiales were absent microbiota. Administration Clostridiales, not Bacteroidales, protected from pathogen infection abrogated intestinal...

10.1126/science.aag2029 article EN Science 2017-04-20

Abstract Background Non-alcoholic liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome, and it can progress to non-alcoholic steatohepatitis (NASH). Alterations in gut microbiome have been implicated development NAFLD/NASH, although underlying mechanisms remain unclear. Results We found that consumption prebiotic inulin markedly ameliorated phenotype including steatosis fibrosis, mice. Inulin resulted global changes microbiome, concomitant enrichment genera Bacteroides...

10.1186/s40168-021-01125-7 article EN cc-by Microbiome 2021-09-16

Gut microbiota act beyond the gastrointestinal tract to regulate physiology of host. However, their contribution antioxidant capacity host remains largely understudied. In this study, we observe that gut bacteria increase steady-state plasma levels high-antioxidant molecules, reactive sulfur species (RSS), such as hydrogen sulfide and cysteine persulfide (CysSSH), in Moreover, utilize cystine a substrate enzymatically produce CysSSH. Administration mice increases RSS suppresses...

10.1016/j.celrep.2022.110479 article EN cc-by Cell Reports 2022-03-01

Abstract Mesothelial cells that line the serous cavities and outer surface of internal organs are involved in inflammatory responses induced by microbial stimuli bacterial infection. Upon exposure to products, mesothelial secrete chemokines, but signaling pathways which these recognize bacteria mediate innate immune remain largely unknown. We report stimulation primary peritoneal via nucleotide-binding oligomerization domain (Nod)1, a member intracytoplasmic Nod-like receptor family, potent...

10.4049/jimmunol.179.1.514 article EN The Journal of Immunology 2007-07-01

Urticarial rash observed in cryopyrin-associated periodic syndrome (CAPS) caused by nucleotide-binding oligomerization domain–leucine-rich repeats containing pyrin domain 3 (NLRP3) mutations is effectively suppressed anti–interleukin (IL)-1 treatment, suggesting a pathophysiological role of IL-1β the skin. However, cellular mechanisms regulating production skin CAPS patients remain unclear. We identified mast cells (MCs) as main cell population responsible for patients. Unlike normal MCs...

10.1084/jem.20082179 article EN The Journal of Experimental Medicine 2009-04-13

Clostridium difficile is a Gram-positive obligate anaerobic pathogen that causes pseudomembranous colitis in antibiotics-treated individuals. However, host immune protective mechanisms against C. are largely unknown. In this study, we show possesses potent stimulatory activity for nucleotide-binding oligomerization domain 1 (Nod1), an intracellular pattern recognition molecule senses bacterial peptidoglycan-related molecules. Nod1(-/-), but not Nod2(-/-), mice exhibited increased lethality...

10.4049/jimmunol.1003761 article EN The Journal of Immunology 2011-03-17

Nod1 and Nod2 are intracellular proteins that involved in recognition of bacterial molecules their genetic variations have been linked to several inflammatory diseases strongly affected by environmental factors. However, the distribution Nod1- Nod2-stimulatory different species environments is unknown. Here we established a quantitative bioassay screen characterize activities sites species. Using this system, found common including foods soils contain high levels activities. Several Bacillus...

10.1074/jbc.m602638200 article EN cc-by Journal of Biological Chemistry 2006-07-27

Abstract Muramyl dipeptide (MDP), the microbial activator of nucleotide-binding oligomerization domain 2 (Nod2), induces NF-κB and MAPK activation, leading to production multiple anti-bacterial proinflammatory molecules. In addition, MDP has been implicated in IL-1β secretion through regulation caspase-1. However, mechanisms that mediate caspase-1 activation response stimulation remain poorly understood. We show here fluorescent molecules are internalized primary macrophages accumulate...

10.4049/jimmunol.180.6.4050 article EN The Journal of Immunology 2008-03-15

The nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 3 (Nlrp3) inflammasome plays an important role in inflammation by controlling the maturation and secretion of cytokines IL-1β IL-18 response to multiple stimuli including pore-forming toxins, particulate matter, ATP. Although pathways activated latter lead a decrease intracellular K(+) concentration, which is required for activation, mechanism microbial RNA activates Nlrp3, remains poorly understood. In this...

10.4049/jimmunol.1400582 article EN The Journal of Immunology 2014-09-16

Host immunity limits iron availability to pathogenic bacteria, but whether bacteria from accessing host heme, the major source of in body, remains unclear. Using Citrobacter rodentium, a mouse enteric pathogen and Escherichia coli, cause sepsis humans as models, we find that interleukin-22, cytokine best known for its ability promote epithelial barrier function, also suppresses systemic growth by limiting pathogen. an unbiased proteomic approach understand mechanistic basis IL-22 dependent...

10.1126/sciimmunol.aai8371 article EN Science Immunology 2017-02-04
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