Potential Associations Between Microbiome and COVID-19

Abstract

The coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has plunged the world into a major crisis. The disease is characterized by strong infectivity, high morbidity, and high mortality. It is still spreading in some countries. Microbiota and their metabolites affect human physiological health and diseases by participating in host digestion and nutrition, promoting metabolic function, and regulating the immune system. Studies have shown that human microecology is associated with many diseases, including COVID-19. In this research, we first reviewed the microbial characteristics of COVID-19 from the aspects of gut microbiome, lung microbime, and oral microbiome. We found that significant changes take place in both the gut microbiome and airway microbiome in patients with COVID-19 and are characterized by an increase in conditional pathogenic bacteria and a decrease in beneficial bacteria. Then, we summarized the possible microecological mechanisms involved in the progression of COVID-19. Intestinal microecological disorders in individuals may be involved in the occurrence and development of COVID-19 in the host through interaction with ACE2, mitochondria, and the lung-gut axis. In addition, fecal bacteria transplantation (FMT), prebiotics, and probiotics may play a positive role in the treatment of COVID-19 and reduce the fatal consequences of the disease.

Keywords: ACE2; COVID-19; gut-lung axis; microbiota; probiotics.

Figure 1

Schematic diagram of coronavirus disease 2019 (COVID-19) infection and its relationship to the gut-lung axis and microbiome disorders. 1. The destruction of the intestinal barrier integrity by microbial imbalance may lead to the migration of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) from the lungs through the circulatory and lymphatic systems to the intestinal cavity. Conversely, bacterial disorders can lead to the rupture of the intestinal barrier and the migration of SARS-CoV-2 viruses from the intestines to the lungs. 2. ACE2 is widely expressed in intestinal epithelial cells. SARS-CoV-2 can use a variety of host proteases to modify the s protein and ACE2 to promote the binding of SARS-CoV-2 to the receptor. After COVID-19 infection, the protective function of ACE2 is lost, which leads to damage of the RAS signal, aggravation of the inflammatory phenotype, and further aggravation of the systemic “cytokine storm” and tissue damage. The permeability of the intestinal barrier changes and intestinal leakage even occurs. 3. In addition, reactive oxygen species (ROS) produced by mitochondria are involved in the innate immune response and inflammation as targets of pathogens. The excessive production of mitochondrial ROS may affect the ROS signal transduction induced by the flora and regulate intestinal barrier function.