Byung Sik Kim

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.

UNLABELLED: Vibrio vulnificus is a seafood-borne pathogen that destroys the intestinal epithelium, leading to rapid bacterial dissemination and death. The most important virulence factor is the multifunctional-autoprocessing repeats-in-toxin (MARTX) toxin comprised of effector domains in the center region flanked by long repeat-containing regions which are well conserved among MARTX toxins and predicted to translocate effector domains. Here, we examined the role of the repeat-containing regions

ABSTRACT Pathogenic Vibrio species cause diseases in diverse marine animals reared in aquaculture. Since their pathogenesis, persistence, and survival in marine environments are regulated by quorum sensing (QS), QS interference has attracted attention as a means to control these bacteria in aquatic settings. A few QS inhibitors of Vibrio species have been reported, but detailed molecular mechanisms are lacking. Here, we identified a novel, potent, and selective Vibrio QS inhibitor, named QStatin

The marine bacterium <i>Vibrio vulnificus</i> causes food-borne diseases, which may lead to life-threatening septicemia in some individuals. Therefore, identifying virulence factors in <i>V. vulnificus</i> is of high priority. We performed a transcriptome analysis on <i>V. vulnificus</i> after infection of human intestinal HT29-methotrexate cells and found induction of <i>plpA</i>, encoding a putative phospholipase, <i>Vv</i>PlpA. Bioinformatics, biochemical, and genetic analyses demonstrated th

The opportunistic pathogen V. parahaemolyticus is a major causative agent for seafood-borne illness worldwide. It also causes severe vibriosis in aquaculture animals, affecting seafood production with huge economic loss. These issues are getting worse due to the current global warming in oceans, spread of antibiotic resistance, and changes in consumer preference toward ready-to-eat (RTE) food items including seafood. To answer the urgent need for sustainable biocontrol agents against V. parahaem

The nan cluster of Vibrio vulnificus, a food-borne pathogen, consists of two divergently transcribed operons, nanT(PSL)AR and nanEK nagA, required for transport and catabolism of N-acetylneuraminic acid (Neu5Ac). A mutation of nanR abolished the extensive lag phase observed for the bacteria growing on Neu5Ac and increased transcription of nanT(P) and nanE, suggesting that NanR is a transcriptional repressor of both nan operons. Intracellular accumulation of Neu5Ac was dependent on the carbon sou

Many Gram-negative bacterial pathogens directly deliver numerous effector proteins from the bacterium to the host cell, thereby altering the target cell physiology. The already well-characterized effector delivery systems are type III, type IV, and type VI secretion systems. Multifunctional autoprocessing repeats-in-toxin (MARTX) toxins are another effector delivery platform employed by some genera of Gram-negative bacteria. These single polypeptide exotoxins possess up to five effector domains

Vibrio vulnificus infects humans and causes lethal septicemia. The primary virulence factor is a multifunctional-autoprocessing repeats-in-toxin (MARTX) toxin consisting of conserved repeats-containing regions and various effector domains. Recent genomic analyses for the newly emerged V. vulnificus biotype 3 strain revealed that its MARTX toxin has two previously unknown effector domains. Herein, we characterized one of these domains, Domain X (DmXVv ). A structure-based homology search revealed

Vibrio vulnificus is a serious infection linked to climate change. The virulence capacity of these bacteria can vary by gene exchange, resulting in new variants of the primary virulence toxin. In this study, we tested whether the emergence of an epidemic strain of V. vulnificus with a novel toxin variant correlated with a change in virulence. We found that restoring the biotype 3 toxin variant to the putative progenitor-type toxin resulted in dramatically increased virulence, revealing that the

After invading a host, bacterial pathogens secrete diverse protein toxins to disrupt host defense systems. To ensure successful infection, however, pathogens must precisely regulate the expression of those exotoxins because uncontrolled toxin production squanders energy. Furthermore, inappropriate toxin secretion can trigger host immune responses that are detrimental to the invading pathogens. Therefore, bacterial pathogens use diverse transcriptional regulators to accurately regulate multiple e

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 mediate

V. vulnificus is an opportunistic human pathogen that can cause life-threatening sepsis in immunocompromised patients via seafood poisoning or wound infection. Among the toxic substances produced by this pathogen, the MARTX toxin greatly contributes to disease progression by promoting the dysfunction and death of host cells, which allows the bacteria to disseminate and colonize the host. In response to this, host cells mount a counterattack against the invaders by upregulating various defense ge