Abstract
Oxidative stress is a major contributor to the pathogenesis of various inflammatory diseases. Accumulating evidence has shown that oxidative stress is characterized by the overproduction of reactive oxygen species (ROS). Previous reviews have highlighted inflammatory signaling pathways, biomarkers, molecular targets, and pathogenetic functions mediated by oxidative stress in various diseases. The inflammatory signaling cascades are initiated through the recognition of host cell-derived damage associated molecular patterns (DAMPs) and microorganism-derived pathogen associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs). In this review, the effects of PRRs from the Toll-like (TLRs), the retinoic acid-induced gene I (RIG-I)-like receptors (RLRs) and the NOD-like (NLRs) families, and the activation of these signaling pathways in regulating the production of ROS and/or oxidative stress are summarized. Furthermore, important directions for future studies, especially for pathogen-induced signaling pathways through oxidative stress are also reviewed. The present review will highlight potential therapeutic strategies relevant to inflammatory diseases based on the correlations between ROS regulation and PRRs-mediated signaling pathways.
Highlights
Pattern recognition receptors (PRRs) are the primary sensors for host cell-derived damage associated molecular patterns (DAMPs) and microorganism-derived pathogen associated molecular patterns (PAMPs) and can initiate downstream inflammatory response.It has been acknowledged that inflammatory response is a double-edged sword, which can eradicate the invading pathogen and repair tissue damage sometimes but cause acute and chronic inflammatory diseases at other times
All these results support that the associations of genetic variants in NOD2, TLR4, components of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and autophagy genes play the significant roles in the pathogenesis of Inflammatory bowel diseases (IBD)
Oxidative stress is the result of overproduction of oxidative free radicals and reactive oxygen species (ROS)
Summary
Pattern recognition receptors (PRRs) are the primary sensors for host cell-derived damage associated molecular patterns (DAMPs) and microorganism-derived pathogen associated molecular patterns (PAMPs) and can initiate downstream inflammatory response. [2,3], but NLRC4 inflammasome activation and subsequent IL-18 production contribute to gastric inflammation and dampen host defenses during Helicobacter pylori infection [4]. Intracellular overproductions of ROS or RNS can lead to oxidative stress, which result from the imbalance of ROS generation and consumption, and further trigger proinflammatory cascade and chronic inflammation or autoimmune diseases. A variety of factors including environmental factors, dietary components and/or inappropriate immune responses to host antigens trigger an autoimmune attack against the pancreatic β-cell, and ROS release from phagocytes can lead to a failure to resolve inflammation and the amplification of the autoimmune attack against the β cells, which contribute to the progression of the disease [17]. We summarized and highlighted ROS production mediated by PRRdependent pathways, the relationships and internal molecular mechanisms between ROS imbalance and inflammatory diseases, as well as therapeutics strategies against inflammatory diseases based on the correlations between ROS regulation and PRRs-mediated signaling pathways
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