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Staphylococcal α‐toxin synergistically enhances inflammation caused by bacterial components
Author(s) -
Onogawa Tsuyoshi
Publication year - 2002
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2002.tb00566.x
Subject(s) - phagocytosis , toxin , secretion , staphylococcus aureus , microbiology and biotechnology , tumor necrosis factor alpha , biology , proinflammatory cytokine , inflammation , in vivo , immunology , bacteria , endocrinology , genetics
Abstract This study was performed to investigate the in vivo effects of staphylococcal α‐toxin on phagocytosis and the secretion of proinflammatory cytokines at local sites of intraperitoneal toxin‐challenged mice. A dosage of 45 hemolytic units (HU) of α‐toxin induced a marked increase in the peritoneal neutrophil count. The toxin caused a 52% decrease in phagocytosis by peritoneal macrophages, compared with that of control mice receiving Staphylococcus aureus particles alone. However, no effect on phagocytosis in neutrophils was observed. A dosage of 45 HU toxin and the synergistic activity of S. aureus particles strongly induced interleukin (IL) 6 secretion but only mildly induced IL‐1α secretion. The toxin did not induce the secretion of tumor necrosis factor‐α (TNF‐α). Interestingly, S. aureus culture supernatant induced the secretion of TNF‐α in cultured macrophages. These results suggest that α‐toxin damages the primary host defense system by inducing the oversecretion of IL‐1α and IL‐6, but not TNF‐α, via a mechanism that requires the synergistic action of bacterial components.

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