کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1963603 1058481 2013 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Alternative TLRs are stimulated by bacterial ligand to induce TLR2-unresponsive colon cell response
کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Alternative TLRs are stimulated by bacterial ligand to induce TLR2-unresponsive colon cell response
چکیده انگلیسی


• TLR2-ligand porin stimulated TLR1 and TLR4 of TLR2 down-regulated HT-29 cells.
• Porin induced MD-2, the TLR4 co-receptor known for LPS mediated signaling.
• SARM-1 showed central role in TLR signaling for colonic HT-29 cell response.
• Chemokine expression of the colon cells putatively regulated immune cell migration.

Although pathogenic bacteria penetrate colonic cells causing infection, the role of its surface molecules serving as key Toll-like receptor (TLR) ligands and triggering response remains unexplored. We show that TLR2-ligand porin up-regulated TLR4 on HT-29 cells, which the TLR4-ligand LPS could not. TLR1 that co-express with TLR2 got stimulated with TLR4. Besides the two TLRs, MD-2 was expressed revealing that the TLR4 co-receptor is not exclusive for LPS signaling. SARM-1 that mostly down-regulates TLR-signaling, demonstrated central role in signaling by engaging IRF-3 and NF-κB for cell activity. Porin induced type 1 chemokines particularly MCP-3, while porin-stimulated HT-29 culture supernatant displayed PBMC migration, collectively suggesting that the chemokines influence colon and immune cell cross-talk. In TLR2 down-regulated HT-29 cells, we found TLR1 and TLR4 as substitute TLRs to identify porin and orchestrate signaling. Thus, TLR replacement for PAMP recognition demonstrates specificity of ligand·TLR association can compromise and is a necessary alternative for successful execution of immune responses.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 25, Issue 8, August 2013, Pages 1678–1688
نویسندگان
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