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-  2016 

细胞自噬和炎症反应的相互调控与牙周炎
Interaction of autophagy and inflammation in periodontitis

DOI: 10.7518/gjkq.2016.04.019

Keywords: 自噬,炎症,Toll样受体,牙周炎,
autophagy
,inflammation,Toll-like receptor,periodontitis

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Abstract:

摘要: 细胞自噬在真核细胞中广泛存在,其通路可将细胞内衰老损伤的蛋白质和细胞器等细胞成分运送至溶酶体进行降解、清除并循环利用降解后的营养物质。炎症反应是机体应答组织损伤和病原微生物感染等有害刺激的一种保护性反应,过度的炎症反应会导致组织损伤和疾病;而自噬可通过降解DNA、活性氧族等内源性刺激来抑制炎性小体聚集,降解白细胞介素(IL)-1β前体来抑制IL-1β等促炎因子的分泌。牙周致病菌的毒力因子参与牙周组织的破坏,通过其自身携带或释放的脂多糖、肽聚糖和细菌DNA等与宿主细胞的Toll样受体(TLR)等相互作用诱发组织局部炎性细胞浸润和释放炎症因子,导致牙周炎。在牙周局部组织中,病原相关分子模式和损伤相关分子模式通过与TRL或核苷酸结合寡聚化结构域蛋白样受体相互作用,在激活先天免疫反应时诱发自噬,而自噬同时可通过负向调控TLR信号来影响炎症反应。本文就自噬与炎症反应的相互调控作用和自噬与牙周炎的相关性等研究进展作一综述,旨在揭示牙周炎等炎症性疾病的发病机制,为其治疗探索新的途径。
Abstract: In autophagy, damaged proteins, organelles, and nutrients are transported to lysosomes for degradation, elimination, and recycling. This process is a highly conserved mechanism among eukaryotic cells. Inflammation is a vital protective host response to tissue damage and pathogenic infection. However, excessive inflammation can cause tissue damage and diseases. Autophagy inhibits the assembly of inflammasomes by degrading endogenous stimuli, including DNA and reactive oxygen species. This process also controls interleukin(IL)-1β secretion by targeting pro-IL-1β for degradation. Periodontal pathogens destroy periodontal tissues through the interaction of Toll-like receptor(TLR) with various components, such as lipopolysaccharide, peptidoglycan, and bacterial DNA. As a consequence, inflammatory cells are recruited and inflammatory cytokines are released. In local periodontal tissues, TLR or nucleotide-binding oligomerization domain-like receptor activates innate immune responses, induces autophagy-related pathways, and recognizes pathogen- and damage-associated molecular patterns. Autophagy can also influence inflammatory responses by negatively regulating TLR signals. This review focuses on recent progress in the mutual regulation of autophagy and inflammation. This review also describes the potential relations between autophagy and periodontitis to elucidate disease pathogenesis and to develop new therapies

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