https://scholars.lib.ntu.edu.tw/handle/123456789/508162
標題: | Like Cures Like: Pharmacological Activity of Anti-Inflammatory Lipopolysaccharides From Gut Microbiome | 作者: | Lin T.-L. CHIN-CHUNG SHU Chen Y.-M. Lu J.-J. Wu T.-S. Lai W.-F. Tzeng C.-M. HSIN-CHIH LAI Lu C.-C. |
公開日期: | 2020 | 卷: | 11 | 起(迄)頁: | 554 | 來源出版物: | Frontiers in Pharmacology | 摘要: | Gut microbiome maintains local gut integrity and systemic host homeostasis, where optimal control of intestinal lipopolysaccharides (LPS) activity may play an important role. LPS mainly produced from gut microbiota are a group of lipid-polysaccharide chemical complexes existing in the outer membrane of Gram-negative bacteria. Traditionally, LPS mostly produced from Proteobacteria are well known for their ability in inducing strong inflammatory responses (proinflammatory LPS, abbreviated as P-LPS), leading to septic shock or even death in animals and humans. Although the basic structures and chemical properties of P-LPS derived from different bacterial species generally show similarity, subtle and differential immune activation activities are observed. On the other hand, frequently ignored, a group of LPS molecules mainly produced by certain microbiota bacteria such as Bacteroidetes show blunt or even antagonistic activity in initiating pro-inflammatory responses (anti-inflammatory LPS, abbreviated as A-LPS). In this review, besides the immune activation properties of P-LPS, we also focus on the description of anti-inflammatory effects of A-LPS, and their potential antagonistic mechanism. We address the possibility of using native or engineered A-LPS for immune modulation in prevention or even treatment of P-LPS induced chronic inflammation related diseases. Understanding the exquisite interactive relationship between structure-activity correlation of P- and A-LPS not only contributes to molecular understanding of immunomodulation and homeostasis, but also re-animates the development of novel LPS-based pharmacological strategy for prevention and therapy of chronic inflammation related diseases. ? Copyright ? 2020 Lin, Shu, Chen, Lu, Wu, Lai, Tzeng, Lai and Lu. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/508162 | ISSN: | 1663-9812 | DOI: | 10.3389/fphar.2020.00554 | SDG/關鍵字: | bacterium lipopolysaccharide; caspase 11; caspase 4; caspase 5; CD14 antigen; e 5531; elastase; eritoran; gamma interferon; gelatinase A; gelatinase B; heat shock protein 70; immunoglobulin enhancer binding protein; interleukin 13; interleukin 1beta; interleukin 4; interleukin 5; interleukin 6; interleukin 8; lipid A; lipopolysaccharide; lipopolysaccharide binding protein; macrophage elastase; monocyte chemotactic protein 1; mts 01; myeloid differentiation factor 88; protein MD 2; toll like receptor 4; tumor necrosis factor; unclassified drug; unindexed drug; allergy; antagonistic effect; antiinflammatory activity; B lymphocyte; binding affinity; CD8+ T lymphocyte; chronic airway hyperreactivity; colitis; collagen degradation; complex formation; cytokine production; cytokine release; endotoxemia; homeostasis; human; immune response; immunomodulation; immunoreactivity; immunostimulation; inflammation; intestine flora; macrophage; neutrophil; NF kB signaling pathway; nonhuman; protein degradation; protein expression level; protein protein interaction; protein structure; respiratory tract disease; Review; signal transduction; site directed mutagenesis; TLR4 MyD88 signaling pathway; TLR4 signaling pathway |
顯示於: | 醫學檢驗暨生物技術學系 |
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