Heat Shock Protein SSA1 Enriched in Hypoxic Secretome of Exerts an Immunomodulatory Effect via Regulating Macrophage Function.

is an opportunistic pathogenic yeast that can survive in both normoxic and hypoxic environments. The involvement of secretome on host biological processes has been demonstrated. However, the immunoregulatory function of secretome released under hypoxic condition remains unclear.

Extracellular vesicles from Staphylococcus aureus promote the pathogenicity of Pseudomonas aeruginosa.

Co-infections with Staphylococcus aureus and Pseudomonas aeruginosa are common in patients with chronic wounds, but little is known about their synergistic effect mediated by extracellular vesicles (EVs). In this study, we investigated the effect of EVs derived from S. aureus (SaEVs) on the pathogenicity of P.

The new 222-nm far ultraviolet-C lowers bacterial contamination to endoscopists during esophagogastroduodenoscopy.

Objectives: This study aimed to clarify the disinfectant efficacy of the 222-nm far ultraviolet-C (UV-C) during esophagogastroduodenoscopy using bacterial cultures.

Methods: The endoscopists performed esophagogastroduodenoscopy wearing a gown with a tryptic soy agar medium plate on their epigastric region and were divided into two groups: 222-nm far UV-C irradiation (UV group) and non-UV irradiation (non-UV group). As a control group, tryptic soy agar medium plates were placed about 110 cm above the floor.

Differential proteomic analysis and pathogenic effects of outer membrane vesicles derived from Acinetobacter baumannii under normoxia and hypoxia.

Acinetobacter baumannii is a major causative agent of nosocomial infections and its outer membrane vesicles (AbOMVs) have been shown to be involved in pathogenicity by transporting virulence factors and transferring information for communication between pathogens and host cells. Despite the fact that the infected sites of A. baumannii such as lungs and skin soft tissues are hypoxic, most studies on AbOMV virulence have used AbOMVs prepared under aerobic conditions.

Effect of ultraviolet C emitted from KrCl excimer lamp with or without bandpass filter to mouse epidermis.

It has been reported that 222-nm ultraviolet C (UVC) exerts a germicidal effect on bacteria and viruses as well as UV radiation emitted from a conventional germicidal lamp but is less toxic to the mammalian cells than that from a germicidal lamp. An excimer lamp filled with krypton chloride (KrCl) gas principally emits 222-nm UVC. However, the lamp also emits a wide band of wavelengths other than 222 nm, especially UVC at a longer wavelength than 222 nm and ultraviolet B, which cause DNA damage.

Extracellular vesicles from methicillin resistant stimulate proinflammatory cytokine production and trigger IgE-mediated hypersensitivity.

Extracellular vesicles (EVs) released from bacteria are enclosed particles carrying biological active molecules. They have been shown to play a role in bacterial communications and delivery of virulence factors to the host cells. is an opportunistic pathogen causing a variety of infections ranging from impetigo to septicaemia.

222-nm UVC inactivates a wide spectrum of microbial pathogens.

Background: UVC has been used to inactivate several pathogens. Unlike the conventional 254-nm UVC, 222-nm UVC is harmless to mammalian cells.

Aim: To investigate the disinfection efficacy of 222-nm UVC against human pathogens which are commonly found in the environment and healthcare facilities.

Interleukin-10 (IL-10) Produced by Mutant Toxic Shock Syndrome Toxin 1 Vaccine-Induced Memory T Cells Downregulates IL-17 Production and Abrogates the Protective Effect against Staphylococcus aureus Infection.

Development of long-term memory is crucial for vaccine-induced adaptive immunity against infectious diseases such as infection. Toxic shock syndrome toxin 1 (TSST-1), one of the superantigens produced by , is a possible vaccine candidate against infectious diseases caused by this pathogen. We previously reported that vaccination with less toxic mutant TSST-1 (mTSST-1) induced T helper 17 (Th17) cells and elicited interleukin-17A (IL-17A)-mediated protection against infection 1 week after vaccination.

Histamine release from intestinal mast cells induced by staphylococcal enterotoxin A (SEA) evokes vomiting reflex in common marmoset.

Staphylococcal enterotoxins (SEs) produced by Staphylococcus aureus are known as causative agents of emetic food poisoning. We previously demonstrated that SEA binds with submucosal mast cells and evokes mast cell degranulation in a small emetic house musk shrew model. Notably, primates have been recognized as the standard model for emetic assays and analysis of SE emetic activity.

Chronic irradiation with 222-nm UVC light induces neither DNA damage nor epidermal lesions in mouse skin, even at high doses.

Surgical site infections (SSIs) represent an important clinical problem associated with increased levels of surgical morbidity and mortality. UVC irradiation during surgery has been considered to represent a possible strategy to prevent the development of SSI. 254-nm UVC induces marked levels of DNA damage by generating cyclobutyl pyrimidine dimers (CPD) in microorganisms.

Contribution of toxic shock syndrome toxin-1 to systemic inflammation investigated by a mouse model of cervicovaginal infection with Staphylococcus aureus.

Toxic shock syndrome toxin-1 (TSST-1), a superantigen produced by Staphylococcus aureus is a causative agent of toxic shock syndrome (TSS) that is frequently associated with tampon use. It has long been suggested that TSS is induced when TSST-1 circulates through the body. However, the systemic distribution of TSST-1 from vagina or uterus has never been demonstrated.

Salmon cartilage proteoglycan promotes the healing process of -infected wound.

Wound healing is the critical event for maintaining skin function and barrier. Inflammatory state in which a variety of cells are activated and accumulated is important for wound healing. Bacterial infection in cutaneous wound is a common problem and causes delay of wound healing.

Disinfection and healing effects of 222-nm UVC light on methicillin-resistant Staphylococcus aureus infection in mouse wounds.

UVC radiation is known to be highly germicidal. However, exposure to 254-nm-UVC light causes DNA lesions such as cyclobutane pyrimidine dimers (CPD) in human cells, and can induce skin cancer after long-term repeated exposures. It has been reported that short wavelength UVC is absorbed by proteins in the membrane and cytosol, and fails to reach the nucleus of human cells.

IL-17A plays an important role in protection induced by vaccination with fibronectin-binding domain of fibronectin-binding protein A against Staphylococcus aureus infection.

Fibronectin-binding protein A (FnBPA) of Staphylococcus aureus is a microbial surface component recognizing adhesive matrix molecules and has been known as one of the most important virulence factors involved in the initiation step of S. aureus infection. Therefore, it has been considered as a potential vaccine candidate.

Passive immunization with anti-ActA and anti-listeriolysin O antibodies protects against Listeria monocytogenes infection in mice.

Listeria monocytogenes is an intracellular pathogen that causes listeriosis. Due to its intracellular niche, L. monocytogenes has evolved to limit immune recognition and response to infection.

Identification and Characterization of a Novel Staphylococcal Emetic Toxin.

Staphylococcal enterotoxins (SEs) produced by Staphylococcus aureus have superantigenic and emetic activities, which cause toxic shock syndrome and staphylococcal food poisoning, respectively. Our previous study demonstrated that the sequence of SET has a low level of similarity to the sequences of other SEs and exhibits atypical bioactivities. Hence, we further explored whether there is an additional SET-related gene in S.

Vaccination with non-toxic mutant toxic shock syndrome toxin-1 induces IL-17-dependent protection against Staphylococcus aureus infection.

Toxic shock syndrome toxin-1 (TSST-1) is one of superantigens produced by Staphylococcus aureus. We have previously demonstrated that vaccination with non-toxic mutant TSST-1 (mTSST-1) develops host protection to lethal S. aureus infection in mice.

Role of interleukin-17A in cell-mediated protection against Staphylococcus aureus infection in mice immunized with the fibrinogen-binding domain of clumping factor A.

Clumping factor A (ClfA) is a fibrinogen-binding cell wall-attached protein and an important virulence factor of Staphylococcus aureus. Previous studies reported that an immunization with the fibrinogen-binding domain of ClfA (ClfA(40-559)) protected animals against S. aureus infection.

c-di-GMP as a vaccine adjuvant enhances protection against systemic methicillin-resistant Staphylococcus aureus (MRSA) infection.

Cyclic diguanylate (c-di-GMP) is a novel immunomodulator and immune enhancer that triggers a protective host innate immune response. The protective effect of c-di-GMP as a vaccine adjuvant against Staphylococcus aureus infection was investigated by subcutaneous (s.c.

Intranasal immunization of mutant toxic shock syndrome toxin 1 elicits systemic and mucosal immune response against Staphylococcus aureus infection.

We investigated whether an intranasal immunization with mutant toxic shock syndrome toxin 1 (TSST-1) could elicit a protective effect against nasal colonization as well as systemic infection of Staphyloccoccus aureus in a mouse model. Anti-TSST-1 antibody production in the mucosal exudates and in sera was efficiently induced. Bacterial numbers were reduced in spleen, liver and also nasal cavities in the early stage of nasal colonization, and the survival rate was significantly improved in the immunized mice.

Intranasal vaccination with a double mutant of staphylococcal enterotoxin C provides protection against Staphylococcus aureus infection.

Staphylococcus aureus expresses a repertoire of factors including staphylococcal exotoxins (SEs), exoenzymes, and numerous cell-associated components that contribute to the pathogenesis of disease. We constructed and expressed a nontoxic double mutant SEC (dmSEC), devoid of superantigenic activity, and investigated the ability of intranasal vaccination with dmSEC plus cholera toxin (CT) adjuvant to protect mice against S. aureus infection.