Abstract
A new infectious disease, named COVID-19, caused by the coronavirus associated to severe acute respiratory syndrome (SARS-CoV-2) has become pandemic in 2020. The three most common pre-existing comorbidities associated with COVID-19-related death are elderly, diabetic, and hypertensive people. A common factor among these risk groups for the outcome of death in patients infected with SARS-CoV-2 is dysbiosis, with an increase in the proportion of bacteria with a pro-inflammatory profile. Due to this dysbiosis, elderly, diabetic, and hypertensive people present a higher propensity to mount an inflammatory environment in the gut with poor immune editing, culminating in a weakness of the intestinal permeability barrier and high bacterial product translocation to the bloodstream. This scenario culminates in a low-grade, persistent, and systemic inflammation. In this context, we propose here that high circulating levels of bacterial products, like lipopolysaccharide (LPS), can potentiate the SARS-CoV-2-induced cytokines, including IL-6, being crucial for development of the cytokine storm in the severe form of the disease. A better understanding on the possible correlation between gut dysbiosis and poor outcomes observed in elderly, diabetic, and hypertensive people can be useful for the development of new therapeutic strategies based on modulation of the gut microbiota.
Highlights
In early December 2019, a new infectious disease, caused by the coronavirus associated to severe acute respiratory syndrome (SARS-CoV-2), emerged in Wuhan, China [1]
Mice and humans exposed to a high salt challenge showed depletion of Lactobacillus spp. in the gut microbiome along with the rise of T helper 17 (Th17) cells and blood pressure (BP) [35], indicating an association of Th17 cells produced by gut microbiota and the generation of hypertension
Since severe COVID-19 patients show high expression of toll-like receptor 4 (TLR4) in peripheral blood mononuclear cells (PBMC) [133], we can speculate that the activation of this receptor by LPS derived from the gut microbiota of elderly, diabetic, and hypertensive individuals would potentiate the production of interleukin 6 (IL-6) induced by SARS-CoV-2
Summary
In early December 2019, a new infectious disease, caused by the coronavirus associated to severe acute respiratory syndrome (SARS-CoV-2), emerged in Wuhan, China [1]. The possibility that SARS-CoV-2 infection of enterocytes modify gut microbiota is supported by the fact that some patients with COVID-19 present intestinal dysbiosis [16, 17]. Diabetic animals treated with probiotics containing the Lactobacillus rhamnosus NCDC17 improved the parameters regarding oral glucose tolerance test and led to an increase in plasma insulin, together with decreased the inflammatory cytokines IL-6 and TNF in the epididymal fat [114].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
