title: Staphylococcus aureus infection induced redox signaling and DNA fragmentation in T-lymphocytes: possible ameliorative role of nanoconjugated vancomycin.
abstract: 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 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 aim of the present study was to test the protective role of nanoconjugated vancomycin against Vancomycin Sensitive S. aureus (VSSA) and Vancomycin Resistant S. aureus (VRSA) infection induced oxidative stress in T-lymphocytes. VSSA and VRSA infection were developed in Swiss mice by intraperitoneal injection of 5 × 10(6) CFU/ml bacterial solutions. Nanoconjugated vancomycin was treated to VSSA and VRSA infected mice at a dose of 100 mg/kg bw/day and 500 mg/kg bw/day, respectively for successive 10 days. Vancomycin was treated to VSSA and VRSA infected mice at similar dose, respectively, for 10 days. The result of this study reveals that in vivo VSSA and VRSA infection significantly increases the level of nitrite generation, lipid peroxidation, protein oxidation, oxidized glutathione level, DNA fragmentation, and decreases the level of reduced glutathione, antioxidant enzyme status, glutathione dependent enzymes as compared to control group; which were increased or decreased significantly near to normal in T-lymphocytes of nanoconjugated vancomycin treated group. These finding suggests the potential use and beneficial protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced oxidative stress in T-lymphocytes.
authors.affiliation: Immunology and Microbiology Laboratory, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, West Bengal, India.
authors.forename: Subhankari Prasad
authors.initials: SP
authors.lastname: Chakraborty
authors.forename: Sabyasachi
authors.initials: S
authors.lastname: Das
authors.forename: Sourav
authors.initials: S
authors.lastname: Chattopadhyay
authors.forename: Satyajit
authors.initials: S
authors.lastname: Tripathy
authors.forename: Sandeep Kumar
authors.initials: SK
authors.lastname: Dash
authors.forename: Panchanan
authors.initials: P
authors.lastname: Pramanik
authors.forename: Somenath
authors.initials: S
authors.lastname: Roy
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D002626:Chemistry, Pharmaceutical; D053938:DNA Fragmentation; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051379:Mice; D058726:Nanoconjugates; D009566:Nitrates / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects*; D013203:Staphylococcal Infections / Q000188:drug therapy* / Q000276:immunology / Q000382:microbiology; D013211:Staphylococcus aureus / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology / Q000382:microbiology; D013997:Time Factors; D014640:Vancomycin / Q000494:pharmacology*; D020713:Vancomycin Resistance
chemical_list: D000900:Anti-Bacterial Agents; D058726:Nanoconjugates; D009566:Nitrates; D014640:Vancomycin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione