Gut microbiota in COVID-19: new insights from inside

Abstract

The epidemic of coronavirus disease-19 (COVID-19) has grown to be a global health threat. Gastrointestinal symptoms are thought to be common clinical manifestations apart from a series of originally found respiratory symptoms. The human gut harbors trillions of microorganisms that are indispensable for complex physiological processes and homeostasis. Growing evidence demonstrate that gut microbiota alteration is associated with COVID-19 progress and severity, and post-COVID-19 syndrome, characterized by decrease of anti-inflammatory bacteria like Bifidobacterium and Faecalibacterium and enrichment of inflammation-associated microbiota including Streptococcus and Actinomyces. Therapeutic strategies such as diet, probiotics/prebiotics, herb, and fecal microbiota transplantation have shown positive effects on relieving clinical symptoms. In this article, we provide and summarize the recent evidence about the gut microbiota and their metabolites alterations during and after COVID-19 infection and focus on potential therapeutic strategies targeting gut microbiota. Understanding the connections between intestinal microbiota and COVID-19 would provide new insights into COVID-19 management in the future.

Keywords: COVID-19; fecal microbiota transplantation; gut microbiota; microbiota-gut-lung axis; probiotics.

Figure 1.

The role of gut microbiota in the pathogenies of COVID-19. Gut microbiota alteration contributes to immune dysfunction and severe disease in COVID-19 course. ACE2 in the gastrointestinal and respiratory tracts mediates SARS-COV-2 entry into the human body and subsequently triggers microbiota alteration and barrier function impairment in the gut and lung. Gut microbiota alteration is characterized by enrichment of inflammation-associated bacteria and decrease of SCFAs-producing bacteria. Gut microbiota alteration and barrier disruption provide opportunities for bacteria translocation, LPS and pro-inflammatory factors increase, SCFAs and secondary BAs and DAT decrease, taken together resulting in intestinal inflammation. Depleted commensal metabolites influence activation of MAIT cells in the host. Intestinal bacteria and inflammatory factors transfer into the blood and cause bacteremia and systemic inflammation. In the lung, microbiota alteration and barrier disruption increase LPS levels and trigger respiratory inflammation. COVID-19, coronavirus disease-19; SARS-CoV-2, severe acute respiratory syndrome coronavirus-2; SCFAs, short-chain fatty acids; DAT, desaminotyrosine; BAs, bile acids; LPS, lipopolysaccharide; ACE2, angiotensin converting enzyme 2; DCs, dendritic cells; LYMs, lymphocytes; Mφs, macrophages; MAIT, mucosal associated invariant T.