کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3355765 1591577 2011 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
TLR2 enhances NADPH oxidase activity and killing of Staphylococcus aureus by PMN
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
TLR2 enhances NADPH oxidase activity and killing of Staphylococcus aureus by PMN
چکیده انگلیسی

Toll-like receptors play an essential role in the detection of invading pathogens. TLR2 is expressed in high concentrations on neutrophils and has been implicated as a critical mediator inducing host antimicrobial defenses against Gram-positive bacteria. Neutrophil responses induced via TLR2 are likely to have important clinical consequences, since Gram-positive organisms, such as Staphylococcus aureus, are an increasingly important source of severe infections. In the present study, we report that TLR2 has a central role in killing of S. aureus by murine PMN via enhancement of NADPH oxidase activity. PMN from TLR2-deficient mice showed a similar inability to kill S. aureus in vitro and under in vivo-like conditions as PMN with a non-functional NADPH oxidase. This defect in killing by TLR2-deficient PMN was not related to phagocytosis but caused by delayed and reduced NADPH oxidase-mediated production of superoxide anion in response to S. aureus and other Gram-positive bacteria. The cause of this was independent of PI3K- and p38 signaling. The TLR2-enhanced induction of superoxide was a defect in proper NADPH oxidase assembly. We hypothesize that early activation of TLR2-signaling may enhance p47phox phosphorylation subsequent to phagocytosis-mediated phosphorylation. Summarized, these data demonstrate a novel role of TLR2 in the killing of S. aureus by ensuring a rapid activation of the NADPH oxidase complex.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunology Letters - Volume 135, Issues 1–2, 30 March 2011, Pages 17–23
نویسندگان
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