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題名 | Molecular Mechanisms in Lipopolysaccharide-Induced Interleukin 6 Release in Lymphatic Endothelial Cells=脂多醣體誘導淋巴內皮細胞IL-6釋放之機轉 |
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作者 | 許文憲; 楊弘宇; 邱佩婷; 許銘仁; | 書刊名 | Journal of Food and Drug Analysis |
卷期 | 19:3 2011.09[民100.09] |
頁次 | 頁245-251+377 |
分類號 | 415.13 |
關鍵詞 | 人類淋巴內皮細胞; 脂多醣體; 蛋白激酶MAPK; 轉錄因子; Lymphatic endothelial cells; LECs; Lipopolysaccharide; LPS; Mitogen-activated protein kinases; MAPKs; Transcription factor; NF-κB; |
語文 | 英文(English) |
英文摘要 | ABSTRACT The lymphatic vasculature is involved in the transportation of tissue fluids, extravasated plasma proteins and cells back into blood circulation. Formation of lymphatic vessels by lymphatic endothelial cells (LECs) occurs both in normal tissues as well as in pathological processes including inflammation, lymphedema and tumor metastasis. Recent reports demonstrated that lymphatic vasculature is not just a major conduit for immune cell transport. It seems to be directly involved in both the induction and the resolution of inflammation. However, little is known about how lymphatic vessels themselves respond to inflammation. The purpose of this study was to investigate the molecular mechanism by which interleukin-6 release in LECs exposure to lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria. LPS was shown to cause an increase in IL-6 release in LECs. Pharmacological inhibitors of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK), p38MAPK or c-jun N-terminal kinase (JNK), significantly abrogated the LPS-induced IL-6 release. In addition, LPS was shown to activate ERK, p38MAPK and JNK in LECs, suggesting functional crosstalk. The results of reporter assay further indicated that LPS increased the transcriptional activity of NF-κB, a critical transcription factor in inducing IL-6 expression. Our data suggest that MAPKs and NF-κB activation may contribute to LPS-induced IL-6 release in LECs. Interventions of MAPKs and NF-κB signaling may be beneficial in the treatment of lymphatic-associated inflammation. |
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