Treponema denticola stimulates Oncostatin M cytokine release and de novo synthesis in neutrophils and macrophages.
Treponema denticola stimulates Oncostatin M cytokine release and de novo synthesis in neutrophils and macrophages.
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DOI：
10.1002/jlb.4ma0620-072rr
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发表时间：
2020-11
影响因子：
5.5
通讯作者：
Visser MB
中科院分区：
文献类型：
--
作者：
Jones MM;Vanyo ST;Ibraheem W;Maddi A;Visser MB
抑瘤素M（OSM）是一种多效性细胞因子，在包括牙周病在内的许多炎症性疾病中升高。OSM由多种免疫细胞产生，具有多种功能，如调节代谢过程、细胞分化和对细菌病原体的炎症反应。由于持续存在的共生细菌，口腔处于持续的免疫监视下，包括互补的中性粒细胞和巨噬细胞群体。牙周病的特点是一个生态失调的细菌群落，与大量的密螺旋体denticola。尽管与严重的牙周病密切相关，但OSM在口腔中的释放来源和机制尚未确定。我们发现OSM蛋白在牙周病期间在牙龈上皮和免疫细胞浸润中升高。此外，唾液和口腔中性粒细胞OSM升高与T的存在相关。齿垢在气囊感染模型中，T.齿垢刺激的OSM水平高于口腔病原体牙龈卟啉单胞菌，尽管先天性免疫细胞的不同募集提示T。齿垢具有提高OSM水平的独特特性。OSM的释放和转录在暴露于T.如通过ELISA、qPCR和显微镜所测量的，在体外对龋齿进行了检测。通过转录、翻译和肌动蛋白聚合抑制，我们发现T。齿垢刺激中性粒细胞中通过脱粒和从头合成的OSM释放以及巨噬细胞中的OSM释放和合成。T.齿垢可能促进临床牙周病。先天免疫细胞遇到T。齿垢差异诱导OSM促进牙周病期间牙龈炎症。
Oncostatin M (OSM) is a pleiotropic cytokine elevated in a number of inflammatory conditions including periodontal disease. OSM is produced by a variety of immune cells and has diverse functionality such as regulation of metabolic processes, cell differentiation and the inflammatory response to bacterial pathogens. The oral cavity is under constant immune surveillance including complementary neutrophil and macrophage populations, due to a persistent symbiotic bacterial presence. Periodontal disease is characterized by a dysbiotic bacterial community, with an abundance of Treponema denticola. Despite strong associations with severe periodontal disease, the source and mechanism of release of OSM has not been defined in the oral cavity. We show that OSM protein is elevated in the gingival epithelium and immune cell infiltrate during periodontal disease. Furthermore, salivary and oral neutrophil OSM is elevated in correlation with the presence of T. denticola. In an air pouch infection model, T. denticola stimulated higher levels of OSM than the oral pathogen Porphorymonas gingivalis despite differential recruitment of innate immune cells suggesting T. denticola has distinct properties to elevate OSM levels. OSM release and transcription was increased in isolated human blood, oral neutrophils or macrophages exposed to T. denticola in vitro as measured by ELISA, qPCR and microscopy. Using transcription, translation, and actin polymerization inhibition, we found that T. denticola stimulates both OSM release through degranulation and de novo synthesis in neutrophils and also OSM release and synthesis in macrophages. Differential induction of OSM by T. denticola may promote clinical periodontal disease. Innate immune cells which encounter T. denticola differentially induce OSM to promote gingival inflammation during periodontal disease.
影响因子：
3.7
作者：
Abiko Y;Nagano K;Yoshida Y;Yoshimura F
通讯作者：
Yoshimura F