Journal of Microbiology

Ju-Hyung Lee

2 Articles

Host–microbial interactions in metabolic diseases: from diet to immunity: Ju-Hyung Lee , Joo-Hong Park; J. Microbiol. 2022;60(6):561-575. Published online May 5, 2022; DOI: https://doi.org/10.1007/s12275-022-2087-y

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Growing evidence suggests that the gut microbiome is an important contributor to metabolic diseases. Alterations in microbial communities are associated with changes in lipid metabolism, glucose homeostasis, intestinal barrier functions, and chronic inflammation, all of which can lead to metabolic disorders. Therefore, the gut microbiome may represent a novel therapeutic target for obesity, type 2 diabetes, and nonalcoholic fatty liver disease. This review discusses how gut microbes and their products affect metabolic diseases and outlines potential treatment approaches via manipulation of the gut microbiome. Increasing our understanding of the interactions between the gut microbiome and host metabolism may help restore the healthy symbiotic relationship between them.

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Metabolites.2022; 12(8): 687. CrossRef

A mucin-responsive hybrid two-component system controls Bacteroides thetaiotaomicron colonization and gut homeostasis: Ju-Hyung Lee , Soo-Jeong Kwon , Ji-Yoon Han , Sang-Hyun Cho , Yong-Joon Cho , Joo-Hong Park; J. Microbiol. 2022;60(2):215-223. Published online February 1, 2022; DOI: https://doi.org/10.1007/s12275-022-1649-3

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Abstract PDF

The mammalian intestinal tract contains trillions of bacteria. However, the genetic factors that allow gut symbiotic bacteria to occupy intestinal niches remain poorly understood. Here, we identified genetic determinants required for Bacteroides thetaiotaomicron colonization in the gut using transposon sequencing analysis. Transposon insertion in BT2391, which encodes a hybrid two-component system, increased the competitive fitness of B. thetaiotaomicron. The BT2391 mutant showed a growth advantage in a mucin-dependent manner and had an increased ability to adhere to mucus-producing cell lines. The increased competitive advantage of the BT2391 mutant was dependent on the BT2392–2395 locus containing susCD homologs. Deletion of BT2391 led to changes in the expression levels of B. thetaiotaomicron genes during gut colonization. However, colonization of the BT2391 mutant promoted DSS colitis in low-fiber diet-fed mice. These results indicate that BT2391 contributes to a sustainable symbiotic relationship by maintaining a balance between mucosal colonization and gut homeostasis.

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