However, because our bodies are inhabited by trillions of mostly beneficial bacteria, virus and fungi, activation of our immune response is tightly regulated to distinguish between harmful and helpful microbes.
In these chronic diseases, the gut microbiome lacks bacteria that activate immune cells that block the response against harmless bacteria in our guts.
A fraction of patients infected with SARS-CoV-2, the virus that causes COVID-19 disease, develop severe complications that require hospitalization in intensive care units?
The COVID-19 pandemic has inspired me to shift my research and explore the role of the gut microbiome in the overly aggressive immune response against SARS-CoV-2 infection.
My colleagues and I have hypothesized that critically ill SARS-CoV-2 patients with conditions like obesity, Type 2 diabetes and cardiovascular disease exhibit an altered gut microbiome that aggravates acute respiratory distress syndrome.
Acute respiratory distress syndrome, a life-threatening lung injury, in SARS-CoV-2 patients is thought to develop from a fatal overreaction of the immune response called a cytokine storm that causes an uncontrolled flood of immune cells into the lungs.
Several studies described in one recent review have identified an altered gut microbiome in patients with COVID-19.
However, identification of specific bacteria within the microbiome that could predict COVID-19 severity is lacking.
We collected stool and saliva samples to determine whether bacteria within the gut and oral microbiome could predict COVID-19 severity.
The identification of microbiome markers that can predict the clinical outcomes of COVID-19 disease is key to help prioritize patients needing urgent treatment.
But it is not yet clear from our research what is the contribution of the altered microbiome in the immune response to SARS-CoV-2 infection.
Thus, researchers like me need to take repeated patient stool, saliva and blood samples over a longer time frame to learn how the altered microbiome observed in COVID-19 patients can modulate COVID-19 disease severity, perhaps by altering the development of the T-regulatory cells.