tetano
Editor, Senior Moderator
Obes Med
. 2020 Dec;20:100302.
doi: 10.1016/j.obmed.2020.100302. Epub 2020 Sep 18.
Gut microbiome dysbiosis and endotoxemia - Additional pathophysiological explanation for increased COVID-19 severity in obesity
Andrej Belančić[SUP] 1 [/SUP]
Affiliations
Abstract
The overall intestinal lipopolysaccharide (LPS) composition in the individuals with obesity could be shifted away from immunosilent/immunoinhibitory Bacteroidetes 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.
Keywords: Coronavirus; Endotoxin; Gut microbiota; High-fat diet; Lipopolysaccharide; Obesity.
. 2020 Dec;20:100302.
doi: 10.1016/j.obmed.2020.100302. Epub 2020 Sep 18.
Gut microbiome dysbiosis and endotoxemia - Additional pathophysiological explanation for increased COVID-19 severity in obesity
Andrej Belančić[SUP] 1 [/SUP]
Affiliations
- PMID: 32984641
- PMCID: PMC7500405
- DOI: 10.1016/j.obmed.2020.100302
Abstract
The overall intestinal lipopolysaccharide (LPS) composition in the individuals with obesity could be shifted away from immunosilent/immunoinhibitory Bacteroidetes 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.
Keywords: Coronavirus; Endotoxin; Gut microbiota; High-fat diet; Lipopolysaccharide; Obesity.