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作 者:任静宜 刘歆婵[1] 丁烨[1] 于洪强[1] 周延民[1] 于维先
机构地区:[1]吉林大学口腔医院种植中心 [2]吉林省牙发育及颌骨重塑与再生省重点实验室,长春130021
出 处:《国际口腔医学杂志》2016年第4期462-467,共6页International Journal of Stomatology
基 金:吉林省卫生厅资助项目(20102045);吉林省发改委资助项目(2013C022-4);吉林省科技厅资助项目(20150101076JC)~~
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。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. Infl ammation 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 infl uence infl ammatory responses by negatively regulating TLR signals. This review focuses on recent progress in the mutual regulation of autophagy andinflammation. This review also describes the potential relations between autophagy and periodontitis to elucidate disease pathogenesis and to develop new therapies.
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