Nagoya University · Medicine
Professor Yoshio Araki's research lab specializes in glycobiology and host-microbe interactions, with a focus on the structural chemistry of bacterial cell walls, particularly peptidoglycan and teichoic acids in Gram-positive bacteria. The lab investigates enzymatic deacetylation of chitin and chitin derivatives, exploring the roles of these enzymes in microbial metabolism and host immune responses. A central theme is the pathogenesis of inflammatory bowel disease (IBD), using DSS-induced colitis models to dissect the contributions of intestinal mast cells, microbiota, and short-chain fatty acids to mucosal inflammation and barrier integrity. The lab also examines bioactive food components, such as germinated barley foodstuffs, in modulating colonic inflammation through microbial and metabolic pathways.
Figures are computed from collected data and may differ slightly.
1. An enzyme that catalyzes hydrolysis of acetamido groups of chitin derivatives was found in the supernatant fraction of Mucor rouxii. 2. Partially O-hydroxyethylated chitin (glycol chitin) was used as a substrate in the purification and characterization of this enzyme. A 140-fold purification was obtained by means of ammonium sulfate fractionation followed by chromatography on carboxymethylcellulose and DEAE-cellulose. 3. The enzyme releases about 30% of the acetyl groups of glycol chitin, giv
The occurrence of N-nonsubstituted glucosamine residues in Bacillus cereus cell wall peptidoglycan is demonstrated and accounts for resistance of the cell walls to lysozyme. Lysozyme-resistant cell walls isolated from three strains of B.cereus indicate unusually small free muramic acid contents as analyzed in an autoanalyzer after acid hydrolysis. Over 80% of the total muramic acid was recovered from the acid hydrolysates of the peptidoglycan as disaccharides, which were identified as glucosamin
Pathogenic mechanisms responsible for inflammatory bowel disease (IBD) are poorly understood. In an IBD animal model, the oral administration of polysaccharides such as dextran sulfate sodium (DSS) induces colitis, which exhibit several clinical and histological features for IBD. However, pathogenic factors in the development of colitis remain unclear. Therefore, we investigated possible mechanisms for DSS-induced colitis, and mainly focused on biological responses from an intestinal epithelial
Article de synthese sur la structure chimique de la jonction entre le peptidoglycane et les polyosides (acides teichoiques, acides teichuroniques et autres polyosides) dans la paroi des bacteries Gram positif
Ws/Ws rats have a small deletion of the c-kit gene, and are deficient in both mucosal-type mast cells (MMC) and connective tissue-type mast cells (CTMC). In the present study we investigated the role of intestinal MMC in the development of dextran sulphate sodium (DSS)-induced experimental colitis using Ws/Ws rats. Ws/Ws and control (+/+) rats were given a 3% DSS aqueous solution orally for 10 days, and the subsequent mucosal damage was evaluated macroscopically and histologically. The mucosal m
Germinated barley foodstuff (GBF) administration has been previously reported to suppress dextran sulfate sodium (DSS)-induced experimental colitis. In this study, we investigated the roles of the intestinal microflora and short chain fatty acids (SCFAs) following administration of GBF in DSS-induced rat colitis. Sprague-Dawley rats were fed 3% (w/w of diet) DSS in GBF-diets for 5 days. The control rats were fed 3% DSS in cellulose-diets for 5 days. The administration of GBF effectively prevente
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