Journal of Microbiology

Editorial

Pioneering strategies for overcoming bacterial drug resistance: Byoung Sik Kim; J. Microbiol. 2026;64(3):e2603100. Published online March 31, 2026; DOI: https://doi.org/10.71150/jm.2603100

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Review

Bacterial Sialic Acid Catabolism at the Host–Microbe Interface: Jaeeun Kim , Byoung Sik Kim; J. Microbiol. 2023;61(4):369-377. Published online March 27, 2023; DOI: https://doi.org/10.1007/s12275-023-00035-7

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Sialic acids consist of nine-carbon keto sugars that are commonly found at the terminal end of mucins. This positional feature of sialic acids contributes to host cell interactions but is also exploited by some pathogenic bacteria in evasion of host immune system. Moreover, many commensals and pathogens use sialic acids as an alternative energy source to survive within the mucus-covered host environments, such as the intestine, vagina, and oral cavity. Among the various biological events mediated by sialic acids, this review will focus on the processes necessary for the catabolic utilization of sialic acid in bacteria. First of all, transportation of sialic acid should be preceded before its catabolism. There are four types of transporters that are used for sialic acid uptake; the major facilitator superfamily (MFS), the tripartite ATP-independent periplasmic C4-dicarboxilate (TRAP) multicomponent transport system, the ATP binding cassette (ABC) transporter, and the sodium solute symporter (SSS). After being moved by these transporters, sialic acid is degraded into an intermediate of glycolysis through the well-conserved catabolic pathway. The genes encoding the catabolic enzymes and transporters are clustered into an operon(s), and their expression is tightly controlled by specific transcriptional regulators. In addition to these mechanisms, we will cover some researches about sialic acid utilization by oral pathogens.

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Article

Vibrio vulnificus PlpA facilitates necrotic host cell death induced by the pore forming MARTX toxin: Changyi Cho , Sanghyeon Choi , Myung Hee Kim , Byoung Sik Kim; J. Microbiol. 2022;60(2):224-233. Published online February 1, 2022; DOI: https://doi.org/10.1007/s12275-022-1448-x

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Abstract PDF

Opportunistic pathogen Vibrio vulnificus causes severe systemic infection in humans with high mortality. Although multiple exotoxins have been characterized in V. vulnificus, their interactions and potential synergistic roles in pathogen-induced host cell death have not been investigated previously. By employing a series of multiple exotoxin deletion mutants, we investigated whether specific exotoxins of the pathogen functioned together to achieve severe and rapid necrotic cell death. Human epithelial cells treated with V. vulnificus with a plpA deletion background exhibited an unusually prolonged cell blebbing, suggesting the importance of PlpA, a phospholipase A2, in rapid necrotic cell death by this pathogen. Additional deletion of the rtxA gene encoding the multifunctional autoprocessing repeats-in-toxin (MARTX) toxin did not result in necrotic cell blebs. However, if the rtxA gene was engineered to produce an effector-free MARTX toxin, the cell blebbing was observed, indicating that the pore forming activity of the MARTX toxin is sufficient, but the MARTX toxin effector domains are not necessary, for the blebbing. When a recombinant PlpA was treated on the blebbed cells, the blebs were completely disrupted. Consistent with this, MARTX toxin-pendent rapid release of cytosolic lactate dehydrogenase was significantly delayed in the plpA deletion background. Mutations in other exotoxins such as elastase, cytolysin/hemolysin, and/or extracellular metalloprotease did not affect the bleb formation or disruption. Together, these findings indicate that the pore forming MARTX toxin and the phospholipase A2, PlpA, cooperate sequentially to achieve rapid necrotic cell death by inducing cell blebbing and disrupting the blebs, respectively.

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Research Support, Non-U.S. Gov't

Identification and Characterization of the Vibrio vulnificus rtxA Essential for Cytotoxicity in vitro and Virulence in Mice: Jeong Hyun Lee , Myung Won Kim , Byoung Sik Kim , Seung Min Kim , Byung Cheol Lee , Tae Sung Kim , Sang Ho Choi; J. Microbiol. 2007;45(2):146-152.; DOI: https://doi.org/2520 [pii]

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Abstract PDF: A mutant exhibiting decreased cytotoxic activity toward INT-407 intestinal epithelial cells and carrying a mutation in the rtx gene cluster that consists of rtxCA and rtxBDE operons was screened from a library of V. vulnificus mutants. The functions of the rtxA gene, assessed by constructing an isogenic mutant and evaluating its phenotypic changes, demonstrated that RtxA is essential for the virulence of V. vulnificus in mice as well as in tissue cultures.

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