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staphylococcal infections/glutathione
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Immunization with glutathione S-transferase and mutant toxic shock syndrome toxin 1 fusion protein protects against Staphylococcus aureus infection.
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To investigate whether immunization with glutathione S-transferase (GST) and mutant toxic shock syndrome toxin 1 (mTSST-1) fusion protein can protect against Staphylococcus aureus infection, we purified a non-toxic mutant GST-mTSST-1 fusion protein. Mice were immunized with the GST-mTSST-1 plus alum
In vitro dose and duration dependent approaches for the assessment of ameliorative effects of nanoconjugated vancomycin against Staphylococcus aureus infection induced oxidative stress in murine peritoneal macrophages.
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OBJECTIVE
The present study was aimed to evaluate the in vitro ameliorative effect of nanoconjugated vancomycin (NV) against vancomycin sensitive and resistant strains of Staphylococcus aureus infection-induced oxidative stress in murine peritoneal macrophage.
METHODS
Peritoneal macrophages from
Staphylococcus aureus Infection Induced Oxidative Imbalance in Neutrophils: Possible Protective Role of Nanoconjugated Vancomycin.
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Staphylococcus aureus infection causes oxidative stress in neutrophils. The immune cells use reactive oxygen species (ROS) for carrying out their normal functions while an excess amount of ROS can attack cellular components that lead to cell damage. The present study was aimed to test the protective
Protective effect of glutathione S-transferase-fused mutant staphylococcal enterotoxin C against Staphylococcus aureus-induced bovine mastitis.
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Recent studies have demonstrated that immunization with nontoxic mutant staphylococcal enterotoxin C (mSEC) provides protection against Staphylococcus aureus infection in mouse models. In the present study, we investigated whether vaccination with a glutathione S-transferase-fused SEC (GST-mSEC) can
Efficacy of two novel 2,2'-bifurans to inhibit methicillin-resistant Staphylococcus aureus infection in male mice in comparison to vancomycin.
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The therapeutic efficacy of two novel bifurans and vancomycin in an animal model of a methicillin-resistant Staphylococcus aureus (MRSA) infection was compared. Adult male CF-1 mice (25-35 g) were intraperitoneally injected with 200 μL/mouse containing 10(7) cell-forming units of MRSA. After 16
Staphylococcus aureus infection induced redox signaling and DNA fragmentation in T-lymphocytes: possible ameliorative role of nanoconjugated vancomycin.
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Staphylococcus aureus is most frequently isolated pathogen causing bloodstream infections, skin and soft tissue infections and pneumonia. Vancomycin sensitive and resistant S. aureus infection causes oxidative stress in neutrophils and lymphocytes. Lymphocyte is an important immune cell. The immune
Ampicillin alone and in combination with riboflavin modulates Staphylococcus aureus infection induced septic arthritis in mice.
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Effects of ampicillin (Amp) in combination with riboflavin on septic arthritis in mice infected with Staphylococcus aureus have been reported. Ampicillin was given at 100 mg/kg after 24 h of infection, followed by riboflavin (Ribo) at 20 mg/kg body wt, after 2 h of Amp treatment. Mice were
[Antioxidants and immunomodulating action of antibiotics and antibiotic-treated erythrocytes in staphylococcal infections].
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Staphylococcus infection inhibited the T-dependent immune response, increased the serum levels of the lipid peroxidation products (LPP) i.e. fatty acid diene conjugates and malonic aldehyde and lowered the activity of the antioxidant system enzymes (ASE) i.e. superoxide dismutase and glutathione
Gentamicin in combination with ascorbic acid regulates the severity of Staphylococcus aureus infection-induced septic arthritis in mice.
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To study the effects of gentamicin in combination with ascorbic acid on septic arthritis, mice were infected with Staphylococcus aureus (S. aureus) and treated with gentamicin, which was given at 5 mg/kg after 24 h of infection, followed by ascorbic acid, given at 20 mg/kg body weight after 2 h of
Azithromycin in combination with riboflavin decreases the severity of Staphylococcus aureus infection induced septic arthritis by modulating the production of free radicals and endogenous cytokines.
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OBJECTIVE
To determine alternate therapeutic measures to combat Staphylococcus aureus induced arthritis. Thus, azithromycin was combined with riboflavin, which may combat the ROS production and inflammation.
METHODS
An in vivo model of S. aureus infection-induced arthritis was set up by infecting
Riboflavin along with antibiotics balances reactive oxygen species and inflammatory cytokines and controls Staphylococcus aureus infection by boosting murine macrophage function and regulates inflammation.
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BACKGROUND
Macrophages serve as intracellular reservoirs of S. aureus. Recent in vitro studies have confirmed high level resistance by S. aureus to macrophage mediated killing and the intracellular persistence of Staphylococci may play an important role in the pathogenesis. Since this localization
Pathogen and autoantigen homologous regions within the cystic fibrosis transmembrane conductance regulator (CFTR) protein suggest an autoimmune treatable component of cystic fibrosis.
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The cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel provides the glutathione and hypochlorous acid necessary for bactericidal/viricidal actions. CFTR mutations block these effects, diminishing pathogen defence and allowing extracellular pathogen accumulation, where
Staphylococcal cell membrane antigen, a possible antigen in post-methicillin resistant Staphylococcus aureus (MRSA) infection nephritis and IgA nephropathy, exhibits high immunogenic activity that is enhanced by superantigen.
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BACKGROUND
The post-methicillin resistant Staphlylococcus aureus (MRSA) infection nephritis is a progressive glomerulonephritis that occurs following Staphylococcus aureus infection. It has been assumed that staphylococcal superantigens and other cellular antigens are necessary for the development
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