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Periodontitis and cardiometabolic disorders: The role of lipopolysaccharide and endotoxemia
Periodontology 2000 ( IF 18.6 ) Pub Date : 2022-03-04 , DOI: 10.1111/prd.12433
Pirkko J Pussinen 1 , Elisa Kopra 1 , Milla Pietiäinen 1 , Markku Lehto 2, 3, 4 , Svetislav Zaric 5 , Susanna Paju 1 , Aino Salminen 1
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Lipopolysaccharide is a virulence factor of gram-negative bacteria with a crucial importance to the bacterial surface integrity. From the host's perspective, lipopolysaccharide plays a role in both local and systemic inflammation, activates both innate and adaptive immunity, and can trigger inflammation either directly (as a microbe-associated molecular pattern) or indirectly (by inducing the generation of nonmicrobial, danger-associated molecular patterns). Translocation of lipopolysaccharide into the circulation causes endotoxemia, which is typically measured as the biological activity of lipopolysaccharide to induce coagulation of an aqueous extract of blood cells of the assay. Apparently healthy subjects have a low circulating lipopolysaccharide activity, since it is neutralized and cleared rapidly. However, chronic endotoxemia is involved in the pathogenesis of many inflammation-driven conditions, especially cardiometabolic disorders. These include atherosclerotic cardiovascular diseases, obesity, liver diseases, diabetes, and metabolic syndrome, where endotoxemia has been recognized as a risk factor. The main source of endotoxemia is thought to be the gut microbiota. However, the oral dysbiosis in periodontitis, which is typically enriched with gram-negative bacterial species, may also contribute to endotoxemia. As endotoxemia is associated with an increased risk of cardiometabolic disorders, lipopolysaccharide could be considered as a molecular link between periodontal microbiota and cardiometabolic diseases.

中文翻译:

牙周炎和心脏代谢疾病:脂多糖和内毒素血症的作用

脂多糖是革兰氏阴性菌的毒力因子,对细菌表面的完整性至关重要。从宿主的角度来看,脂多糖在局部和全身炎症中都发挥作用,激活先天免疫和适应性免疫,并且可以直接(作为与微生物相关的分子模式)或间接(通过诱导产生非微生物、危险-相关的分子模式)。脂多糖易位进入循环导致内毒素血症,其通常被测量为脂多糖诱导测定的血细胞水提取物凝固的生物活性。显然,健康受试者的循环脂多糖活性较低,因为它被迅速中和并清除。然而,慢性内毒素血症与许多炎症驱动疾病的发病机制有关,尤其是心脏代谢疾病。这些包括动脉粥样硬化性心血管疾病、肥胖、肝病、糖尿病和代谢综合征,其中内毒素血症已被认为是危险因素。内毒素血症的主要来源被认为是肠道微生物群。然而,牙周炎中的口腔菌群失调,通常富含革兰氏阴性菌,也可能导致内毒素血症。由于内毒素血症与心脏代谢疾病的风险增加有关,脂多糖可以被认为是牙周微生物群和心脏代谢疾病之间的分子联系。这些包括动脉粥样硬化性心血管疾病、肥胖、肝病、糖尿病和代谢综合征,其中内毒素血症已被认为是危险因素。内毒素血症的主要来源被认为是肠道微生物群。然而,牙周炎中的口腔菌群失调,通常富含革兰氏阴性菌,也可能导致内毒素血症。由于内毒素血症与心脏代谢疾病的风险增加有关,脂多糖可以被认为是牙周微生物群和心脏代谢疾病之间的分子联系。这些包括动脉粥样硬化性心血管疾病、肥胖、肝病、糖尿病和代谢综合征,其中内毒素血症已被认为是危险因素。内毒素血症的主要来源被认为是肠道微生物群。然而,牙周炎中的口腔菌群失调,通常富含革兰氏阴性菌,也可能导致内毒素血症。由于内毒素血症与心脏代谢疾病的风险增加有关,脂多糖可以被认为是牙周微生物群和心脏代谢疾病之间的分子联系。通常富含革兰氏阴性细菌,也可能导致内毒素血症。由于内毒素血症与心脏代谢疾病的风险增加有关,脂多糖可以被认为是牙周微生物群和心脏代谢疾病之间的分子联系。通常富含革兰氏阴性细菌,也可能导致内毒素血症。由于内毒素血症与心脏代谢疾病的风险增加有关,脂多糖可以被认为是牙周微生物群和心脏代谢疾病之间的分子联系。
更新日期:2022-03-04
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