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Extracellular vesicles of P. gingivalis-infected macrophages induce lung injury
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease ( IF 4.2 ) Pub Date : 2021-08-11 , DOI: 10.1016/j.bbadis.2021.166236
Kayo Yoshida 1 , Kaya Yoshida 2 , Natsumi Fujiwara 1 , Mariko Seyama 1 , Kisho Ono 3 , Hotaka Kawai 4 , Jiajie Guo 5 , Ziyi Wang 6 , Yao Weng 7 , Yaqiong Yu 5 , Yoko Uchida-Fukuhara 7 , Mika Ikegame 7 , Akira Sasaki 3 , Hitoshi Nagatsuka 4 , Hiroshi Kamioka 6 , Hirohiko Okamura 7 , Kazumi Ozaki 1
Affiliation  

Periodontal diseases are common inflammatory diseases that are induced by infection with periodontal bacteria such as Porphyromonas gingivalis (Pg). The association between periodontal diseases and many types of systemic diseases has been demonstrated; the term “periodontal medicine” is used to describe how periodontal infection/inflammation may impact extraoral health. However, the molecular mechanisms by which the factors produced in the oral cavity reach multiple distant organs and impact general health have not been elucidated. Extracellular vesicles (EVs) are nano-sized spherical structures secreted by various types of cells into the tissue microenvironment, and influence pathophysiological conditions by delivering their cargo. However, a detailed understanding of the effect of EVs on periodontal medicine is lacking. In this study, we investigated whether EVs derived from Pg-infected macrophages reach distant organs in mice and influence the pathophysiological status. EVs were isolated from human macrophages, THP-1 cells, infected with Pg. We observed that EVs from Pg-infected THP-1 cells (Pg-inf EVs) contained abundant core histone proteins such as histone H3 and translocated to the lungs, liver, and kidneys of mice. Pg-inf EVs also induced pulmonary injury, including edema, vascular congestion, inflammation, and collagen deposition causing alveoli destruction. The Pg-inf EVs or the recombinant histone H3 activated the NF-κB pathway, leading to increase in the levels of pro-inflammatory cytokines in human lung epithelial A549 cells. Our results suggest a possible mechanism by which EVs produced in periodontal diseases contribute to the progression of periodontal medicine.



中文翻译:

牙龈卟啉单胞菌感染巨噬细胞的细胞外囊泡诱导肺损伤

牙周病是由感染牙周病菌如感应共炎性疾病卟齿龈小号PG)。牙周病与许多类型的全身性疾病之间的关联已被证明;“牙周病医学”一词用于描述牙周感染/炎症如何影响口腔外健康。然而,口腔中产生的因子到达多个远处器官并影响整体健康的分子机制尚未阐明。细胞外囊泡 (EVs) 是由各种类型的细胞分泌到组织微环境中的纳米级球形结构,并通过传递其货物来影响病理生理条件。然而,缺乏对电动汽车对牙周医学影响的详细了解。在这项研究中,我们研究了源自Pg感染巨噬细胞的EV 是否到达小鼠的远处器官并影响病理生理状态。从感染Pg 的人巨噬细胞 THP-1 细胞中分离出 EV 我们观察到来自Pg感染的 THP-1 细胞 ( Pg -inf EVs) 的 EVs 含有丰富的核心组蛋白,如组蛋白 H3,并易位到小鼠的肺、肝和肾。Pg- inf EVs 还会引起肺损伤,包括水肿、血管充血、炎症和导致肺泡破坏的胶原蛋白沉积。的PG -INF电动汽车或重组组蛋白H3激活NF-κB途径,导致促炎细胞因子在人肺上皮A549细胞水平增加。我们的研究结果表明,牙周病中产生的 EV 促进牙周医学发展的可能机制。

更新日期:2021-08-13
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