کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10767463 | 1050733 | 2007 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibition of lipid A-mediated type I interferon induction by Bactericidal/permeability-increasing protein (BPI)
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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![عکس صفحه اول مقاله: Inhibition of lipid A-mediated type I interferon induction by Bactericidal/permeability-increasing protein (BPI) Inhibition of lipid A-mediated type I interferon induction by Bactericidal/permeability-increasing protein (BPI)](/preview/png/10767463.png)
چکیده انگلیسی
Lipopolysaccharide (LPS), a major constituent of the outer membrane of gram-negative bacteria, consists of polysaccharides and a lipid structure named lipid A. Lipid A is a typical microbial pattern molecule that serves as a ligand for Toll-like receptor 4 (TLR4). TLR4 signals the presence of lipid A to recruit adaptor molecules and induces cytokines and type I interferon (IFN) by activating transcription factor, NF-κB or IRF-3. Here we showed that chemically synthesized TLR4-agonistic lipid A analogues but not antagonistic lipid A activate IFN-β promoter in TLR4-expressing HEK293 cells. The amplitude of IFN-β promoter activation was in parallel with that of NF-κB. LPS-binding protein (LBP) was required for efficient IFN-β induction in this system, and this LBP activity was antagonized by bactericidal/permeability-increasing protein (BPI). Thus, we first show that BPI blocks the TLR4 responses by exogenous administration of BPI to lipid A-sensitive cells. Although the functional mechanism whereby extra-cellular BPI modulates the intra-cellular signal pathways selected by the TLR adaptors, MyD88 and TICAM-1 (TRIF), remains unknown, we infer that the lipid A portion of LPS participates in LBP-amplified IFN-β induction and that BPI binding to LPS leads to inhibition of the activation of NF-κB and IFN-β by LPS or agonistic lipid A via TLR4 in an extrinsic mode. BPI may serve as a therapeutic potential against endotoxin shock by acting as a regulator for the MyD88- and TICAM-1 pathways in the LPS-TLR4 signaling.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 354, Issue 2, 9 March 2007, Pages 574-578
Journal: Biochemical and Biophysical Research Communications - Volume 354, Issue 2, 9 March 2007, Pages 574-578
نویسندگان
Masahiro Azuma, Aya Matsuo, Yukari Fujimoto, Koichi Fukase, Kaoru Hazeki, Osamu Hazeki, Misako Matsumoto, Tsukasa Seya,