title: Neutralization of MMP-2 protects Staphylococcus aureus infection induced septic arthritis in mice and regulates the levels of cytokines.
abstract: Matrix metalloproteinases (MMPs) are crucial players in Staphylococcus aureus mediated synovial tissue destruction in the pathogenesis of septic arthritis. Bacterial insult increases proteolytic matrix fragments by activated chondrocytes and synovial fibroblasts leading to induction of matrix metalloproteinases. Tissue destruction via MMPs induced by bacterial products, necrotic tissues and proinflammatory cytokines have been reported. Cytokines like TNF-α, IL-1β released from host cells in response to S. aureus infection promote cartilage degradation by stimulating the production of MMPs. Antibiotic treatment can eradicate invading bacteria but elevated levels of cytokines and cytokines induced MMPs activation lead to progressive and devastating bone and cartilage destruction even after bacterial clearance. Like other MMPs, MMP-2 also contributes to extracellular matrix degradation in different types of arthritis. Release of certain pro inflammatory cytokines can also be regulated by MMP-2 activation leading to further tissue destruction. The role of MMP-2 in the pathogenesis of S. aureus infection induced septic arthritis and its influence on cytokines regulation needs further investigation. Whether neutralization of MMP-2 provides protection against Staphylococcus aureus infection induced septic arthritis in mice is an obvious question. Here we reported that neutralization of MMP-2 during S. aureus infection induced septic arthritis might be beneficial for preventing infection induced extracellular matrix destruction thereby decreasing bacterial burden in synovial tissues and regulating inflammatory cytokines in arthritic mice.
authors.affiliation: Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, India. Electronic address: sultana.sahin96@gmail.com.
authors.forename: Sahin
authors.initials: S
authors.lastname: Sultana
authors.affiliation: Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, India. Electronic address: rana0489@gmail.com.
authors.forename: Rana
authors.initials: R
authors.lastname: Adhikary
authors.affiliation: Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, India. Electronic address: ajeyan294@gmail.com.
authors.forename: Ajeya
authors.initials: A
authors.lastname: Nandi
authors.affiliation: Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, India. Electronic address: biswa_dev2@yahoo.com.
authors.forename: Biswadev
authors.initials: B
authors.lastname: Bishayi
mesh_terms: D000818:Animals; D001170:Arthritis, Infectious / Q000473:pathology*; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism*; D051379:Mice; D013203:Staphylococcal Infections / Q000473:pathology*; D013211:Staphylococcus aureus / Q000254:growth & development* / Q000276:immunology
chemical_list: D016207:Cytokines; D020778:Matrix Metalloproteinase 2
keywords: Inflammation; MMP-2; S. aureus; Septic arthritis; TNF-α