کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5897108 | 1155257 | 2014 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Pathological activation of canonical nuclear-factor κB by synergy of tumor necrosis factor α and TNF-like weak inducer of apoptosis in mouse acute colitis
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کلمات کلیدی
TLRLPCsTNBSMLNTNF-like weak inducer of apoptosisFn14TWEAKTNF-amAbLPSPBSECs - EC هاTrinitrobenzene sulfonic acid - اسید سولفونیک TrinitrobenzeneToll-like receptor - تیالآرepithelial cell - سلول اپیتلیالepithelial cells - سلول بافت پوششی یا اپیتلیومCytokines - سیتوکین هاnuclear factor - عامل هسته ایtumor necrosis factor - فاکتور نکروز تومورlipopolysaccharide - لیپوپلی ساکاریدPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریMonoclonal antibodies - پادتنهای تَکتیرهAcute colitis - کولیت حادmesenteric lymph node - گره لنفاوی مزانتریک
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
علوم غدد
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چکیده انگلیسی
Tumor necrosis factor (TNF)-α is a major effector in various inflammatory conditions. TNF-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily that promotes inflammatory tissue damage through its receptor, FGF-inducible molecule 14 (Fn14). Since both TWEAK and TNF-α have been shown to mediate pathological responses through inter-dependent or independent pathways by in vitro, the potential interplay of these pathways was investigated in a mouse colitis model. Acute colitis was induced by rectal injection of trinitrobenzene sulfonic acid (TNBS), with administration of control IgG, TNF receptor (TNFR)-Ig chimeric protein, anti-TWEAK monoclonal antibody, or the combination of TNFR-Ig and anti-TWEAK antibody. On day 4, disease severity was evaluated and gene expression profiling was analyzed using whole colon tissue. NF-κB activation was investigated with Western blot. Levels of transcript of TWEAK, Fn14 and NF-κB-related molecules were measured in purified colon epithelial cells (ECs). As a result, activation of the canonical (p50/RelA), but not noncanonical (p100/RelB)-mediated pathway was the hallmark of inflammatory responses in this model. Inflammation induced upregulation of Fn14 only in ECs but not in other cell types. Combination treatment of TNFR-Ig and anti-TWEAK antibody synergistically reduced disease severity in comparison with the control antibody or single agent treatment. Gene expression profile of the colon indicated downregulation of canonical NF-κB pathway with combination treatment. In conclusion, synergistic activation of canonical NF-κB by TWEAK and TNF-α is critical for the induction of inflammatory tissue damage in acute inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cytokine - Volume 69, Issue 1, September 2014, Pages 14-21
Journal: Cytokine - Volume 69, Issue 1, September 2014, Pages 14-21
نویسندگان
Taeko Dohi, Rei Kawashima, Yuki I. Kawamura, Takeshi Otsubo, Teruki Hagiwara, Aldo Amatucci, Jennifer Michaelson, Linda C. Burkly,