Belančić Andrej
Department of Clinical Pharmacology, University Hospital Centre Rijeka, Krešimirova 42, 51000, Rijeka, Croatia.
Obes Med. 2020 Dec;20:100302. doi: 10.1016/j.obmed.2020.100302. Epub 2020 Sep 18.
The overall intestinal lipopolysaccharide (LPS) composition in the individuals with obesity could be shifted away from immunosilent/immunoinhibitory LPS subtypes, in favor of various proinflammatory LPS subtypes due to gut microbiome dysbiosis. What is more, high-fat diet, as well as obesity per se, enhance intestinal permeability through various mechanisms. Latter results in increased paracellular absorption and transcellular (via chylomicrons) transport of endogenous endotoxin in the circulatory system (endotoxemia). In addition, it is known that lipid A initiates a signaling cascade resulting in activation of various proinflammatory pathways and increases oxidative stress upon binding to tool-like receptor 4 (TLR4). Taking everything into consideration, it is very likely that gut microbiome dysbiosis and endotoxemia represent the additional pathophysiological explanation for increased COVID-19 severity in obesity.
由于肠道微生物群失调，肥胖个体的整体肠道脂多糖（LPS）组成可能会从免疫沉默/免疫抑制性LPS亚型发生转变，转而有利于各种促炎性LPS亚型。此外，高脂饮食以及肥胖本身会通过多种机制增强肠道通透性。后者导致循环系统中内源性内毒素的细胞旁吸收和跨细胞（通过乳糜微粒）转运增加（内毒素血症）。此外，已知脂多糖A会引发信号级联反应，导致各种促炎途径的激活，并在与Toll样受体4（TLR4）结合时增加氧化应激。综合考虑所有因素，肠道微生物群失调和内毒素血症很可能是肥胖患者COVID-19病情加重的额外病理生理学解释。
