title: Possible protective role of chloramphenicol in TSST-1 and coagulase-positive Staphylococcus aureus-induced septic arthritis with altered levels of inflammatory mediators.
abstract: Chloramphenicol is mostly used against coagulase-negative Staphylococcus aureus, and its protective role against coagulase-positive S. aureus is not well studied. In our study, arthritis was induced in mice by S. aureus (Apollo Gleneagles 33 (AG-33) or American Type Culture Collection 25923 (ATCC-25923)) infection. Chloramphenicol was administered after 2 h of infection. Mice were killed at 1, 3, 5 days post-infection. Mice inoculated with pathogenic Staphylococci (AG-33) expressing coagulase and Toxic shock syndrome toxin-1 (TSST-1), displayed severe arthritis with enhanced bacterial burden in the spleen, cytokine production in serum and synovial tissue, neutrophil recruitment, and cyclooxegenase-2 expression in synovial tissue compared with ATCC-25923-infected groups. Severity of arthritis was regulated by chloramphenicol treatment. Our study suggests that alteration in the inflammatory cytokine levels and pronounced production of cyclooxygenase-2 play important roles in progression of arthritis which is regulated by application of chloramphenicol.
authors.affiliation: Immunology Laboratory, Department of Physiology, University Colleges of Science and Technology, University of Calcutta, Calcutta, West Bengal 700009, India.
authors.forename: Sayantani
authors.initials: S
authors.lastname: Majumdar
authors.forename: Kallol
authors.initials: K
authors.lastname: Dutta
authors.forename: Sunil K
authors.initials: SK
authors.lastname: Manna
authors.forename: Anirban
authors.initials: A
authors.lastname: Basu
authors.forename: Biswadev
authors.initials: B
authors.lastname: Bishayi
mesh_terms: D000818:Animals; D001170:Arthritis, Infectious / Q000188:drug therapy* / Q000378:metabolism / Q000382:microbiology; D001427:Bacterial Toxins / Q000378:metabolism*; D002701:Chloramphenicol / Q000627:therapeutic use*; D003030:Coagulase / Q000276:immunology / Q000378:metabolism*; D051546:Cyclooxygenase 2 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis / Q000097:blood; D004768:Enterotoxins / Q000378:metabolism*; D018836:Inflammation Mediators / Q000097:blood* / Q000276:immunology; D051379:Mice; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism; D016133:Polymerase Chain Reaction; D013203:Staphylococcal Infections / Q000276:immunology* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000276:immunology* / Q000378:metabolism / Q000472:pathogenicity; D018089:Superantigens / Q000378:metabolism*; D013582:Synovial Fluid / Q000166:cytology; D014527:Uric Acid / Q000097:blood
chemical_list: D001427:Bacterial Toxins; D003030:Coagulase; D016207:Cytokines; D004768:Enterotoxins; D018836:Inflammation Mediators; D018089:Superantigens; C030107:enterotoxin F, Staphylococcal; D014527:Uric Acid; D002701:Chloramphenicol; D051546:Cyclooxygenase 2