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Possible Role of Toll‐like Receptor‐2 in the Intracellular Survival of S taphylococcus aureus in Murine Peritoneal Macrophages: Involvement of Cytokines and Anti‐Oxidant Enzymes
Author(s) -
Bishayi B.,
Bandyopadhyay D.,
Majhi A.,
Adhikary R.
Publication year - 2014
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12195
Subject(s) - microbiology and biotechnology , catalase , tlr2 , phagocytosis , staphylococcus aureus , superoxide dismutase , cytokine , tumor necrosis factor alpha , biology , intracellular , chemistry , receptor , immunology , enzyme , tlr4 , biochemistry , bacteria , genetics
Effects of blocking toll‐like receptor‐2 ( TLR ‐2) on the survival of S taphylococcus aureus ( S . aureus ) and cytokine production in peritoneal macrophages of S wiss albino mice were analysed. Macrophages were infected with S . aureus in the presence and absence of anti‐ TLR ‐2 antibody. Tumour necrosis factor‐ α ( TNF ‐ α ) interleukin‐6 ( IL ‐6), interferon‐gamma ( IFN ‐ γ ), interleukin‐1 β ( IL ‐1 β ), interleukin‐12 ( IL ‐12) and interleukin‐10 ( IL ‐10) concentrations were measured. Expressions of TLR ‐2, NF ‐ κ B , M y D 88 were analysed by W estern B lot. Expression of TLR ‐2 was increased in S . aureus ‐infected macrophages with respect to control and was M y D 88 independent. TLR 2 blocking significantly reduced TNF ‐ α , IL ‐6, IL ‐1 β and IL ‐10 and increased IFN ‐ γ and IL ‐12 production. Decreased catalase activity and increased superoxide dismutase ( SOD ) by S . aureus with concomitant increase in H 2 O 2 and nitric oxide ( NO ) were observed in the case of prior TLR ‐2 blocking. To understand whether catalase contributing in the intracellular survival, was of bacterial origin or not, 3‐amino, 1, 2, 4‐triazole ( ATZ ) was used to inhibit specifically macrophage‐derived catalase. Catalase enzyme activity from the whole staphylococcal cells in the presence of ATZ suggested that the released catalase were of extracellular origin. From the intracellular survival assay, it was evident that pretreatment of macrophages with ATZ reduces the bacterial burden in macrophages when infected with the recovered bacteria only from the anti‐ TLR ‐2 antibody‐treated macrophages after phagocytosis. Catalase protein expression from the whole staphylococcal cells recovered after phagocytosis also indicated the catalase release from S . aureus . Capturing of S . aureus via TLR ‐2 induces inflammatory reactions through activation of NF ‐ κ B‐signalling pathways which was M y D 88‐independent.