Nanoconjugated vancomycin ameliorates Staphylococcus aureus infection induced cellular pathogenesis: an in vitro approach

Abstract

Staphylococcus aureus, the majority recurrently isolated microorganism, is responsible for bloodstream infections, skin and soft tissue infections and pneumonia. S. aureus infection causes cellular oxidative stress in host. Macrophage is an important immunological cell. Generally, for carrying out normal cellular functions, the immunological cells use reactive oxygen species (ROS); but an excess amount of ROS can destroy the cellular components that lead to cell damage or dealth. The present study was aimed to focus on the in vitro protective role of nanoconjugated vancomycin against S. aureus infection-induced cellular oxidative stress and DNA damage. VSSA and VRSA infection was developed in murine peritoneal macrophages by the treatment of 100ml of bacterial suspension containing 5×10⁶ CFU/ml for 3hr. Vancomycin and Nanoconjugated vancomycin was treated to VSSA and VRSA infected macrophages. The result of this study reveals that in vitro VSSA and VRSA infection significantly increases the level of superoxide anion and nitrite generation, NADPH and myeloperoxidase activity, 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 usual in murine peritoneal macrophages of nanoconjugated vancomycin treated group. These finding suggests the potential protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced cellular oxidative stress and DNA damage.