Like Cures Like: Pharmacological Activity of Anti-Inflammatory Lipopolysaccharides From Gut Microbiome
Journal
Frontiers in Pharmacology
Journal Volume
11
Pages
554
Date Issued
2020
Author(s)
Abstract
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.
SDGs
Other Subjects
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
Type
review