Altering gut bacteria levels could help to protect the heart following heart failure.
When the heart becomes compromised to such an extent that it can no longer pump enough blood around the body, it is known as heart failure.
Currently, almost 6 million people in the United States are living with heart failure.
Heart failure is serious, and around half of the people who develop it die within just 5 years.
Understanding how heart failure damages the heart and whether that damage can be prevented is important work. One scientist who is approaching this problem from a unique angle is Francisco J. Carrillo-Salinas, Ph.D., a postdoctoral scholar at Tufts University in Medford, MA.
Gut bacteria, T cells, and heart failure
Carrillo-Salinas is interested in what role the immune system and gut bacteria play in recovery from heart failure.
He explains the main thrust of his work: "Our lab studies how the gut talks to the heart through T cells. Given that the gut is the body's largest reservoir of T cells and microbes, by modulating the microbiota, we could modulate T cell activation and [the] changes in the heart that lead to heart failure."
T cells are a type of white blood cell and play a pivotal role in the immune response. Our resident gut bacteria increase the production of T cells, creating a large stock of these immune cells in our intestines.
His latest study builds on recent findings. For instance, inflammation — a hallmark of the immune response — is already known to play a significant role in heart disease.
To study these relationships further, Carrillo-Salinas turned to a mouse model. Half of the mice had their gut microbes wiped out by a 5-week course of antibiotics and antifungals. Half of this group and half of the group that did not receive antibiotics underwent surgery to mimic the effects of heart failure in humans. Their consequent recovery was charted.
Exterminating gut bacteria
As expected, when compared with the hearts of mice who still had their full microbiome, the hearts of mice without gut bacteria were less damaged and pumped blood more efficiently.
Although the results were in line with expectations — a reduction in the number of T cells infiltrating the heart and reduced cardiac damage — the researchers were impressed by the strength of the effect.
"The fact that we see fully preserved heart function is surprising, and I am looking forward to exciting new data on what happens in the heart once different bacteria recolonize the gut."
Francisco J. Carrillo-Salinas, Ph.D.
The theory is that T cells are activated by heart failure and then move into the heart tissue. Once there, they release cytokines, which are signaling molecules involved in the immune response.
Cytokines cause inflammation and the formation of scar tissue, both of which damage the heart. Without the presence of gut bacteria, there are fewer T cells available, and these changes are prevented.
This is a new and exciting field to be involved in. Carrillo-Salinas explains his fascination:
"Understanding how the gut microbiota directly regulates the function of distant organs such as the heart will shed new light on potential new therapeutic approaches in patients recently diagnosed with heart failure to prevent progression."
These are early days, but this line of investigation could lead to better interventions for those at risk of, or living with, heart failure.
Carrillo-Salinas continues, "Our results demonstrate that gut microbiota depletion prevents cardiac dysfunction and [they] set the stage for future studies that will determine which components of the microbiota are responsible for heart failure progression."