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Porphyromonas gingivalis W83 traffics via ICAM1 in microvascular endothelial cells and alters capillary organization in vivo.
Journal of Oral Microbiology ( IF 4.5 ) Pub Date : 2020-03-26 , DOI: 10.1080/20002297.2020.1742528
L Reyes 1 , H Getachew 2 , W A Dunn 2, 3 , A Progulske-Fox 2
Affiliation  

Objective: Microvascular dysfunction is a feature of periodontal disease. P. gingivalis, one of the most common oral bacteria present in gingival tissue biofilms, has also been identified in the gingival capillaries of patients with chronic periodontitis. We sought to determine the effect of P. gingivalis W83 infection on microvascular endothelium in vivo and in vitro. Methods and Results: Interdental papillae of rats with P. gingivalis-induced alveolar bone loss had a more dilated and denser subepithelial capillary network than uninfected controls. P. gingivalis W83 was detected in the epithelial layers, the subepithelial connective tissue matrix, and subgingival capillaries. P. gingivalis invaded human dermal microvascular endothelial cells (HD-MVECS) and persisted up termination (24 h). Colocalization analysis at 2.5, 6, and 24 h post-inoculation showed that 79-88% of internalized bacteria were in ICAM-1 positive endosomes, and 10-39% were in Rab5, Rab7, or LAMP1 positive compartments, but never in autophagosomes. Antibody-based blockade of ICAM-1 significantly reduced W83 invasion in HD-MVECS. P. gingivalis infected HD-MVECS were unable to form vascular networks in Matrigel. Conclusions: P. gingivalis perturbs microvascular endothelial function and invasion of these cells via ICAM-1 may be important for microbial persistence within tissues.

中文翻译:

牙龈卟啉单胞菌W83通过ICAM1在微血管内皮细胞中运输,并改变体内的毛细血管组织。

目的:微血管功能障碍是牙周疾病的特征。牙龈卟啉单胞菌是存在于牙龈组织生物膜中的最常见的口腔细菌之一,也已在慢性牙周炎患者的牙龈毛细血管中发现。我们试图确定体内和体外牙龈卟啉单胞菌W83感染对微血管内皮的影响。方法和结果:与未感染的对照组相比,牙龈卟啉单胞菌引起的牙槽骨丢失的大鼠的齿间乳头具有更扩张和更密集的上皮下毛细血管网络。在上皮层,上皮下结缔组织基质和龈下毛细血管中检测到了牙龈卟啉单胞菌W83。牙龈卟啉单胞菌侵入人皮肤微血管内皮细胞(HD-MVECS)并持续终止(24 h)。2.5、6时的共定位分析 接种后24小时显示,有79-88%的内在细菌在ICAM-1阳性内体中,有10-39%在Rab5,Rab7或LAMP1阳性内室中,而从未在自噬体中。基于抗体的ICAM-1阻断作用显着降低了HD-MVECS中的W83入侵。牙龈卟啉单胞菌感染的HD-MVECS无法在Matrigel中形成血管网络。结论:牙龈卟啉单胞菌干扰了微血管的内皮功能,这些细胞通过ICAM-1侵入可能对组织内的微生物持久性很重要。牙龈感染的HD-MVECS无法在Matrigel中形成血管网络。结论:牙龈卟啉单胞菌干扰了微血管的内皮功能,这些细胞通过ICAM-1侵入可能对组织内的微生物持久性很重要。牙龈感染的HD-MVECS无法在Matrigel中形成血管网络。结论:牙龈卟啉单胞菌干扰了微血管的内皮功能,这些细胞通过ICAM-1侵入可能对组织内的微生物持久性很重要。
更新日期:2020-04-20
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