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Induction of CC chemokines in human peripheral blood mononuclear cells by staphylococcal exotoxins and its prevention by pentoxifylline
Author(s) -
Krakauer Teresa
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.1.158
Subject(s) - peripheral blood mononuclear cell , biology , pentoxifylline , immunology , peripheral blood , chemokine , microbiology and biotechnology , pharmacology , inflammation , in vitro , biochemistry
We investigated the inflammatory processes that might be associated with the arthrogenic activity of Staphylococcus aureus , the principal causative agent of bacterial arthritis. Human peripheral blood mononuclear cells (PBMC) were stimulated with the staphylococcal toxic shock syndrome toxin‐1 (TSST‐1) or enterotoxin B (SEB) and the production of chemokines was examined. Both TSST‐1 and SEB induced high levels (ng/mL) of MIP‐1α, MIP‐1β, and MCP‐1. The induction of these chemokines occurred mostly by direct stimulation of PBMC with staphylococcal exotoxins (SE), without requiring the intervention of IL‐1 and TNF‐α. The production of SE‐induced chemokines was blocked partially by anti‐DR and anti‐CD2 antibodies. Cell separation revealed monocytes as the cell source of these chemokines. However, addition of purified T cells amplified the levels of chemokine produced, suggesting that cognate interaction of SE bound on antigen‐presenting cells with T cells also contributes to chemokine production. The activation and recruitment of leukocytes by these chemokines may contribute to the pathophysiology of septic arthritis caused by staphylococci in humans through tissue injury and the recruitment of T lymphocytes, perhaps also initiating autoimmune responses. Pentoxifylline, an anti‐inflammatory agent, completely inhibited the production of these chemokines. J. Leukoc. Biol. 66: 158–164; 1999.