Hindawi Publishing Corporation Oxidative Medicine and Cellular Longevity Volume 2011, Article ID 942123, 15 pages doi:10.1155/2011/942123 Research Article Internalization of Staphylococcus aureus in Lymphocytes Induces Oxidative Stress and DNA Fragmentation: Possible Ameliorative Role of Nanoconjugated Vancomycin Subhankari Prasad Chakraborty, 1 Santanu Kar Mahapatra, 1 Sumanta Kumar Sahu, 2 Sabyasachi Das, 1 Satyajit Tripathy, 1 Sandeep Dash, 1 Panchanan Pramanik, 2 and Somenath Roy 1 1 Immunology and Microbiology Laboratory, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore 721 102, India 2 Nanomaterials Laboratory, Department of Chemistry, Indian Institute of Technology, Kharagpur 721 302, India Correspondence should be addressed to Somenath Roy, sroy.vu@hotmail.com Received 7 February 2011; Accepted 7 June 2011 Academic Editor: Kenneth Maiese Copyright © 2011 Subhankari Prasad Chakraborty et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Staphylococcus aureus is the most frequently isolated pathogen causing bloodstream infections, skin and soft tissue infections and pneumonia. Lymphocyte is an important immune cell. The aim of the present paper was to test the ameliorative role of nanoconjugated vancomycin against Vancomycin-sensitive Staphylococcus aureus (VSSA) and vancomycin-resistant Staphylococcus aureus (VRSA) infection-induced oxidative stress in lymphocytes. VSSA and VRSA infections were developed in Swiss mice by intraperitoneal injection of 5 × 10 6 CFU/mL bacterial solutions. Nanoconjugated vancomycin was adminstrated to VSSA- and VRSA-infected mice at its effective dose for 10 days. Vancomycin was adminstrated to VSSA- and VRSA-infected mice at a similar dose, respectively, for 10 days. Vancomycin and nanoconjugated vancomycin were adminstrated to normal mice at their effective doses for 10 days. The result of this study reveals that in vivo VSSA and VRSA infection significantly increases the level of lipid peroxidation, protein oxidation, oxidized glutathione level, nitrite generation, nitrite release, and DNA damage and decreases the level of reduced glutathione, antioxidant enzyme status, and glutathione-dependent enzymes as compared to control group, which were increased or decreased significantly near to normal in nanoconjugated vancomycin-treated group. These findings suggest the potential use and beneficial role of nanoconjugated vancomycin against VSSA and VRSA infection-induced oxidative stress in lymphocytes. 1. Introduction Staphylococcus aureus is a major human pathogen causing significant morbidity and mortality in both community- and hospital-acquired infections [1]. It causes a diverse array of infections ranging from relatively minor skin and wound infections to more serious and life-threatening diseases such as pneumonia, endocarditis, osteomyelitis, arthritis, and sepsis. Concerns over the emergence of multidrug-resistant strains have renewed interest in understanding the virulence mechanisms of this pathogen at the molecular level and in elucidating host defense elements that either provide protection or limit infection [2, 3]. Many staphylococcal infections which tend to become chronic (e.g., osteomyelitis and mastitis) are associated with multiple recurrences and do not resolve even in the presence of what seems to be an adequate humoral immune response [4]. S. aureus has been shown to be ingested by nonprofessional phagocytes, such as mouse fibroblasts, mouse renal cells, and bovine mammary epithelial cells [5, 6]. S. aureus also has the ability to invade mouse and human osteoblast cell lines, as well as normal mouse and human osteoblasts [7, 8]. Polymorphonuclear neutrophils (PMNs) have long been thought to provide significant host defense against S. aureus