炎症
脂质信号
自闭症
免疫学
免疫系统
生物
调解人
细胞生物学
受体
生物化学
作者
Eiba G. Eltay,Thomas E. Van Dyke
标识
DOI:10.1016/j.pharmthera.2023.108453
摘要
The resolution of inflammation is an essential endogenous process that protects host tissues from an exaggerated chronic inflammatory response. Multiple interactions between host cells and resident oral microbiome regulate the protective functions that lead to inflammation in the oral cavity. Failure of appropriate regulation of inflammation can lead to chronic inflammatory diseases that result from an imbalance between pro-inflammatory and pro-resolution mediators. Thus, failure of the host to resolve inflammation can be considered an essential pathological mechanism for progression from the late stages of acute inflammation to a chronic inflammatory response. Specialized pro-resolving mediators (SPMs), which are essential polyunsaturated fatty acid (PUFA)-derived autacoid mediators, aid in regulating the endogenous inflammation resolving process by stimulating immune cell-mediated clearance of apoptotic polymorphonuclear neutrophils, cellular debris, and microbes, restricting further neutrophil tissue infiltration, and counter-regulating pro-inflammatory cytokine production. The SPM superfamily contains four specialized lipid mediator families: lipoxins, resolvins, protectins, and maresins that can activate resolution pathways. Understanding the crosstalk between resolution signals in the tissue response to injury has therapeutic application potential for preventing, maintaining, and regenerating chronically damaged tissues. Here, we discuss the fundamental concepts of resolution as an active biochemical process, novel concepts demonstrating the role of resolution mediators in tissue regeneration in periodontal and pulpal diseases, and future directions for therapeutic applications with particular emphasis on periodontal therapy.
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