Keio University · Biochemistry, Genetics and Molecular Biology
Professor Yun-Gi Kim's research lab focuses on the intricate host-microbiota interactions that shape immune development, metabolic homeostasis, and disease susceptibility. The lab investigates how commensal gut bacteria and microbial metabolites—such as reactive sulfur species, D-amino acids, and short-chain fatty acids—modulate host immunity, oxidative stress responses, and intestinal barrier function. Key research directions include the role of specific bacterial taxa (e.g., Clostridiales, Enterobacteriaceae) in colonization resistance, the immunomodulatory functions of microbial metabolites, and the impact of host pattern recognition receptors (e.g., Nod2) in maintaining gut immune tolerance. The lab integrates gnotobiotic models, metabolomics, and host-pathogen interaction studies to uncover mechanisms underlying inflammatory bowel disease, infection, and metabolic disorders.
Figures are computed from collected data and may differ slightly.
The high susceptibility of neonates to infections has been assumed to be due to immaturity of the immune system, but the mechanism remains unclear. By colonizing adult germ-free mice with the cecal contents of neonatal and adult mice, we show that the neonatal microbiota is unable to prevent colonization by two bacterial pathogens that cause mortality in neonates. The lack of colonization resistance occurred when Clostridiales were absent in the neonatal microbiota. Administration of Clostridial
Gut microbiota act beyond the gastrointestinal tract to regulate the physiology of the host. However, their contribution to the antioxidant capacity of the host remains largely understudied. In this study, we observe that gut bacteria increase the steady-state plasma levels of high-antioxidant molecules, reactive sulfur species (RSS), such as hydrogen sulfide and cysteine persulfide (CysSSH), in the host. Moreover, gut bacteria utilize cystine as a substrate to enzymatically produce CysSSH. Admi
Nucleotide-binding oligomerization domain 2 (Nod2) mutations including L1007fsinsC are associated with the development of Crohn's disease (CD). These CD-associated Nod2 mutations are common in healthy white populations, suggesting that they may confer some protective function, but experimental evidence is lacking. Using a mouse strain that expresses Nod2(2939iCstop), the equivalent of the L1007fsinsC mutation, we found that macrophages homozygous for Nod2(2939iCstop) are impaired in the recognit
Nod2 is an intracellular innate immune receptor that plays a role in host defense and susceptibility to inflammatory disease. We show in this study that macrophages rendered refractory to TLR4 and Nod2 signaling by exposure to LPS and muramyl dipeptide (MDP) exhibit impaired TNF-alpha and IL-6 production in response to pathogenic Listeria monocytogenes and Yersinia pseudotuberculosis as well as commensal bacteria including Escherichia coli and Bacteroides fragilis. Surprisingly, Nod2 deficiency
While poorly-absorbed sugar alcohols such as sorbitol are widely used as sweeteners, they may induce diarrhea in some individuals. However, the factors which determine an individual's susceptibility to sugar alcohol-induced diarrhea remain unknown. Here, we show that specific gut bacteria are involved in the suppression of sorbitol-induced diarrhea. Based on 16S rDNA analysis, the abundance of Enterobacteriaceae bacteria increased in response to sorbitol consumption. We found that <i>Escherichia
<sub>D</sub>-Amino acids (<sub>D</sub>-AAs) have various functions in mammals and microbes. <sub>D</sub>-AAs are produced by gut microbiota and can act as potent bactericidal molecules. Thus, <sub>D</sub>-AAs regulate the ecological niche of the intestine; however, the actual impacts of <sub>D</sub>-AAs in the gut remain unknown. In this study, we show that <sub>D</sub>-Tryptophan (<sub>D</sub>-Trp) inhibits the growth of enteric pathogen and colitogenic pathobionts. The growth of <i>Citrobacter
Metabolic syndrome (MetS) is a multifactorial chronic metabolic disorder that affects approximately one billion people worldwide. Recent studies have evaluated whether targeting the gut microbiota can prevent MetS. This study aimed to assess the ability of dietary fiber to control MetS by modulating gut microbiota composition. Sodium alginate (SA) is a seaweed-derived dietary fiber that suppresses high-fat diet (HFD)-induced MetS via an effect on the gut microbiota. We observed that SA supplemen
A symbiotic relationship between humans and the microbiota is critical for the maintenance of our health, including development of the immune system, enhancement of the epithelial barrier, and acquisition of nutrients. Recent research has shown that the microbiota impacts immune cell development and differentiation. These findings suggest that the microbiota may also influence adjuvant and vaccine efficacy. Indeed, several factors such as malnutrition and poor sanitation, which affect gut microb
Clostridioides difficile causes nosocomial antibiotic-associated diarrhea on a global scale. Susceptibility to C. difficile infection (CDI) is influenced by the composition and metabolism of gut microbiota, which in turn are affected by diet. However, the mechanism underlying the interplay between diet and gut microbiota that modulates susceptibility to CDI remains unclear. Here, we show that a soy protein diet increases the mortality of antibiotic-treated, C. difficile-infected mice while also
Primary dissociated neuronal cultures are widely used research tools to investigate of pathological mechanisms and to treat various central and peripheral nervous system problems including trauma and degenerative neuronal diseases. We introduced a protocol that utilizes hippocampal and cortical neurons from embryonic day 17 or 18 mice. We applied appropriate markers (GAP-43 and synaptophysin) to investigate whether neurite outgrowth and synaptogenesis can be distinguished at a particular period
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