Characterization of Outer Membrane Vesicles Produced by Vibrio vulnificus.

Vibrio vulnificus (V. vulnificus) is a halophilic gram-negative bacterium that inhabits coastal warm water and induce severe diseases such as primary septicemia. To investigate the mechanisms of rapid bacterial translocation on intestinal infection, we focused on outer membrane vesicles (OMVs), which are extracellular vesicles produced by Gram-negative bacteria and deliver virulence factors.

Increased Vascular Permeability Due to Spread and Invasion of in the Wound Infection Exacerbates Potentially Fatal Necrotizing Disease.

is known to cause necrotizing soft tissue infections (NSTIs). However, the pathogenic mechanism causing cellulitis, necrotizing fasciitis, muscle necrosis, and rapidly developing septicemia in humans have not been fully elucidated. Here, we report a multilayer analysis of tissue damage after subcutaneous bacterial inoculation as a murine model of NSTIs.

MukB Is a Gene Necessary for Rapid Proliferation of in the Systemic Circulation but Not at the Local Infection Site in the Mouse Wound Infection Model.

causes rapid septicemia in susceptible individuals who have ingested contaminated foods or have open wounds exposed to seawater contaminated with the bacteria. Despite antibiotic therapy and aggressive debridement, mortality from septicemia is high. In this study, we showed that MukB mutation (::Tn) affected the proliferation of in the systemic circulation but not at the inoculation site in the wound infection model.

New inducible mast cell-deficient mouse model (Mcpt5/Cma1).

Mast cell-deficient mice are helpful for understanding the roles of mast cells in vivo. To date, a dozen mouse models for mast cell deficiency have been reported. However, mice with a specific depletion of all populations of mast cells have not been reported.

Expansion of Necrosis Depending on Hybrid Motor-Driven Motility of in a Murine Wound Infection Model.

The gram-negative bacterium is a cause of fulminant and lethal necrotizing soft tissue infections (NSTIs). Suppressing the rapid proliferation of the pathogen and expansion of the necrosis caused in the host is an important issue in clinical practice, but the pathogenic mechanism for the rapid aggravation has not been clarified. In this study, we characterized the function of two types of motor stators in and explored the role of motility during wound infection.

Transcriptional inhibition of feline immunodeficiency virus by alpha-amanitin.

Alpha-amanitin, one of the amatoxins in egg amanita, has a cyclic peptide structure, and was reported as having antiviral activity against several viruses. We investigated whether α-amanitin has antiviral activity against feline immunodeficiency virus (FIV). FL-4 cells persistently infected with FIV Petaluma were cultured with α-amanitin.

Chemotactic invasion in deep soft tissue by is essential for the progression of necrotic lesions.

Necrotizing soft tissue infections (NSTI) progress to severe necrosis and result in fatal sepsis within a short time. is a causative agent and can spread from the initial infection site through soft tissue finally to the systemic circulation of the host. The motility and chemotaxis of this bacterium are essential for proliferation and lethality in a murine model of the infection, but their role in pathogenicity has not been characterized.

Vibiro vulnificus hemolysin associates with gangliosides.

Background: Vibrio vulnificus hemolysin (VVH) is a pore-forming toxin secreted by Vibrio vulnificus. Cellular cholesterol was believed to be the receptor for VVH, because cholesterol could bind to VVH and preincubation with cholesterol inhibited cytotoxicity. It has been reported that specific glycans such as N-acetyl-D-galactosamine and N-acetyl-D-lactosamine bind to VVH, however, it has not been known whether these glycans could inhibit the cytotoxicity of VVH without oligomer formation.

Functional diversification of two bilin reductases for light perception and harvesting in unique cyanobacterium Acaryochloris marina MBIC 11017.

Bilin pigments play important roles for both light perception and harvesting in cyanobacteria by binding to cyanobacteriochromes (CBCRs) and phycobilisomes (PBS), respectively. Among various cyanobacteria, Acaryochloris marina MBIC 11017 (A. marina 11017) exceptionally uses chlorophyll d as the main photosynthetic pigment absorbing longer wavelength light than the canonical pigment, chlorophyll a, indicating existence of a system to sense longer wavelength light than others.

Identification of Essential Genes of for Establishment of Wound Infection by Signature-Tagged Mutagenesis.

can cause severe necrotic lesions within a short time. Recently, it has been reported that the numbers of wound infection cases in healthy hosts are increasing, for which surgical procedures are essential in many instances to eliminate the pathogen owing to its rapid proliferation. However, the mechanisms by which can achieve wound infection in healthy hosts have not been elucidated.

Accurate prediction of anti-phagocytic activity of Vibrio vulnificus by measurement of bacterial adherence to hydrocarbonsPrediction of Anti-Phagocytic Activity.

Vibrio vulnificus can cause necrotizing soft tissue infection via exposure through an open wound, and the incubation period in cases of wound infection is only about 16 h. These facts strongly suggest that mechanisms to evade innate immune cell phagocytosis are essential for its pathogenicity. Hydrophobic interaction is one of the binding mechanisms between bacteria and phagocytes.

Immunogenicity and protective efficacy of Vibrio vulnificus flagellin protein FlaB in a wound infection model.

Vibrio vulnificus is known as an opportunistic bacterial pathogen that causes primary septicemia and wound infection in humans. Recently, the incidence of wound infection by V. vulnificus is increasing in warm countries.

Both polarity and aromatic ring in the side chain of tryptophan 246 are involved in binding activity of Vibrio vulnificus hemolysin to target cells.

Vibrio vulnificus secretes a hemolysin/cytolysin (VVH) that induces cytolysis against a variety of mammalian cells by forming pores on the cellular membrane. VVH is known to bind to the cellular membrane as a monomer, and then convert to a pore-forming oligomer. However, the structural basis for binding of this toxin to target cells remains unknown.

Importance of fumarate and nitrate reduction regulatory protein for intestinal proliferation of Vibrio vulnificus.

The sepsis caused by Vibrio vulnificus is characterized by an average incubation period of 26 h and a high mortality rate exceeding 50%. The fast growth and dissemination of V. vulnificus in vivo lead to poor clinical outcomes in patients.

A silkworm infection model to investigate Vibrio vulnificus virulence genes.

The halophilic marine bacterium, Vibrio vulnificus, occasionally causes fatal septicemia in immunocompromised patients. Mice are commonly used as experimental animals to investigate the virulence of V. vulnificus, however, a large number of mice are generally required for bioassays.

Are common names becoming less common? The rise in uniqueness and individualism in Japan.

We examined whether Japanese culture has become more individualistic by investigating how the practice of naming babies has changed over time. Cultural psychology has revealed substantial cultural variation in human psychology and behavior, emphasizing the mutual construction of socio-cultural environment and mind. However, much of the past research did not account for the fact that culture is changing.

Vibrio vulnificus detected in the spleen leads to fatal outcome in a mouse oral infection model.

Vibrio vulnificus causes rapid disseminating septicemia by oral infection in infected individuals who have an underlying disease, especially chronic liver diseases. Although the elucidation of specific risk factors for V. vulnificus infection in patients with liver diseases is of urgent importance, no appropriate experimental animal model that mimics the liver diseases in this bacterial infection has been available so far.

Signature-tagged mutagenesis of Vibrio vulnificus.

Vibrio vulnificus is the causative agent of primary septicemia, wound infection and gastroenteritis in immunocompromised people. In this study, signature-tagged mutagenesis (STM) was applied to identify the virulence genes of V. vulnificus.

Comparison of two methods of bacterial DNA extraction from human fecal samples contaminated with Clostridium perfringens, Staphylococcus aureus, Salmonella Typhimurium, and Campylobacter jejuni.

In this study, 2 methods of DNA extraction were evaluated for use in conjunction with the screening system Rapid Foodborne Bacterial Screening 24 (RFBS24), which employs multiplex real-time SYBR Green polymerase chain reaction (SG-PCR) and can simultaneously detect 24 target genes of foodborne pathogens in fecal DNA samples. The QIAamp DNA Stool mini kit (Qkit) and Ultra Clean Fecal DNA Isolation Kit (Ukit) were used for bacterial DNA extraction from fecal samples artificially inoculated with Clostridium perfringens, Staphylococcus aureus, Salmonella Typhimurium, and Campylobacter jejuni. SG-PCR and simplex real-time quantitative PCR (S-qPCR) analyses revealed higher copy numbers (8-234 times) of DNA in samples obtained using Ukit compared with those obtained using Qkit, resulting in lower cycle threshold values for the Ukit samples of the 4 bacteria on SG-PCR analysis.

The Vibrio parahaemolyticus effector VopC mediates Cdc42-dependent invasion of cultured cells but is not required for pathogenicity in an animal model of infection.

Vibrio parahaemolyticus is a Gram-negative marine bacterium that causes acute gastroenteritis in humans. The virulence of V. parahaemolyticus is dependent upon a type III secretion system (T3SS2).

Inhibition of binding of Vibrio vulnificus hemolysin (VVH) by MβCD.

Vibrio vulnificus secrets a pore-forming toxin called Vibrio vulnificus hemolysin (VVH). In this study, we showed that methyl-beta-cyclodextrin (MβCD), an oligosaccharide, decreased binding of VVH to Chinese hamster ovary (CHO) cells, resulting in inhibition of its cytotoxicity. When the VVH was incubated with MβCD, cytotoxicity of the toxin was inhibited from 100.

Immunization with outer membrane protein A from Salmonella enterica serovar Enteritidis induces humoral immune response but no protection against homologous challenge in chickens.

Vaccination of poultry is one promising strategy to mitigate Salmonella infection in poultry and, in turn, humans as well. We evaluated the efficacy of outer membrane protein A (OmpA) as a novel vaccine candidate against Salmonella in poultry. Native OmpA purified from Salmonella enterica serovar Enteritidis was mixed with adjuvant and administered intramuscularly to 41-d-old chicks.