Yonsei University · Medicine
Professor Seung Won Kim's research lab focuses on the interplay between the immune system, microbial dysbiosis, and epithelial barrier integrity in inflammatory diseases, particularly inflammatory bowel disease (IBD). The lab investigates how probiotics, microbial metabolites, and host signaling pathways—such as NF-κB, TLR4, and ER stress—modulate intestinal inflammation and tissue repair. A key research direction involves identifying microbial and host factors that regulate immune homeostasis and tissue regeneration, with translational applications in IBD and chronic mucosal disorders. The lab also explores regenerative mechanisms in epithelial tissues, including tympanic membrane repair, highlighting the role of resident stem cells in tissue repair.
Figures are computed from collected data and may differ slightly.
The results provide insights into the genetic and epigenetic interactions in the IL-23R/IL-17 axis that are associated with elevated expression of IL-17 and IBD pathogenesis.
Our data demonstrate that B. lactis inhibits NF-kappaB and NF-kappaB-regulated genes in IEC and prevents acute colitis and CAC in mice. These results suggest that B. lactis could be a potential preventive agent for CAC as well as a therapeutic agent for inflammatory bowel disease.
Microbial dysbiosis has long been postulated to be associated with the pathogenesis of inflammatory bowel disease (IBD). Although evidence supporting the anti-colitic effects of melatonin have been accumulating, it is not clear how melatonin affects the microbiota. Herein, we investigated the effects of melatonin on the microbiome in colitis and identified involvement of Toll-like receptor (TLR) 4 signalling in the effects. Melatonin improved dextran sulfate sodium (DSS)-induced colitis and reve
An orthotopic model of ATC in athymic nude mice was developed that closely recapitulates the clinical findings of human ATC. This model should facilitate the understanding of the pathogenesis of ATC and aid in the development of novel therapies against ATC.
Tympanic membrane (TM) perforation, in particular chronic otitis media, is one of the most common clinical problems in the world and can present with sensorineural healing loss. Here, we explored an approach for TM regeneration where the latent progenitor or stem cells within TM epithelial layers may play an important regulatory role. We showed that potential TM stem cells present highly positive staining for epithelial stem cell markers in all areas of normal TM tissue. Additionally, they are p
We prove that the averaging formula for Nielsen numbers holds for continuous maps on infra-nilmanifolds: Let M be an infra-nilmanifold and ƒ : M → M be a continuous map. Suppose M K is a regular covering of M which is a compact nilmanifold with π 1 (M K = K . Assume that f * (K) ⊂ K . Then ƒ has a lifting . We prove a question raised by McCord, which is for any with an essential fixed point class, fix =1. As a consequence, we obtain the following averaging formula for Nielsen numbers
Several recent genome-wide association studies (GWAS) identified susceptibility loci/genes for Behçet's disease (BD). However, no study has specifically investigated the genetic susceptibility loci associated with intestinal involvement in BD. We aimed to identify distinctive genetic susceptibility loci/genes associated with intestinal involvement in BD and determine their roles in intestinal inflammation as well as their interactions with genes involved in inflammatory bowel disease (IBD). GWAS
Abstract In this paper we study the averaging formula for Nielsen coincidence numbers of pairs of maps (f,g): M→N between closed smooth manifolds of the same dimension. Suppose that G is a normal subgroup of Π = π 1 (M) with finite index and H is a normal subgroup of Δ = π 1 (N) with finite index such that Then we investigate the conditions for which the following averaging formula holds where is any pair of fixed liftings of ( f, g ). We prove that the averaging formula holds when M and N are o
Open papers in the app to read, cite, and organize with AI.
