Altering our gut bacteria could protect us from the potentially deadly condition sepsis, new research suggests.
By boosting levels of certain gut microbes in mice, researchers at the University of Pennsylvania were able to effectively switch on an immunological shield from the condition.
More and more research suggests that our gut is core to our emotions and immune system, but the new study offers hope that changing our gut could even change the conditions we are susceptible to.
If the findings translate to the human gut, they could help curtail the 15 percent of hundreds of thousands of deaths that sepsis causes each year.
Sepsis might be preventable by encouraging the growth certain gut microbes, a University of Pennsylvania study in mice suggests
Our guts are as unique as our DNA, but infinitely more changeable.
The more we learn about the gut, the more it becomes clear that everything about us shifts as the tiny microorganisms within it do.
Every person has differently-sized populations of each of the trillions of microbes – or microscopic organisms – in our guts.
Depending upon which populations are flourishing in our guts, everything from our digestion to our memories can change, and, according to the new research, so can our response to sepsis.
The body responds to bacterial infections by releasing a wave of chemicals to fight off the invaders.
But the battle has its casualties: inflammation is part of the immune response, and when the fight goes on for too long that inflammation can damage any and all organ systems, a dangerous state called sepsis.
If this state persists, a person is said to be in septic shock, which can result in steep drops in blood pressure and death.
More than one million Americans become septic each year, and between 15 and 30 percent do not survive.
Scientists have noted in the past that people who lack an immune antibody called immunoglobulin A (IgA) have poorer survival rates than others when they get sepsis.
These blood antibodies fight infections without the inflammatory side effects that lead to sepsis.
Certain gut microbes trigger a response from IgA, which then quickly revs up and rushes to the front lines, fighting infection early and lowering the risk of sepsis.
Doctors have had some success treating people with sepsis by giving them IVs of immunoglobulins, and it is thought that those with more IgA are also more resilient against the condition.
But Dr Joel Wilmore and Dr David Allman of the University of Pennsylvania’s Perelman School of Medicine imagined that if they could prompt the body to deploy the antibodies more quickly simply by introducing more of the gut microbes that stimulate that response.
The researchers tested their theory by boosting the levels of a group of microbes in the Proteobacteria phylum.
When they sampled the mice’s blood, they found higher levels of IgA.
So Dr Willmore and Dr Allman went a step further. They induced sepsis in the mice and transferred blood that had no IgA to one group of them.
Only one mouse in that set survived more than two days.
On the other hand, the mice that got the IgA-enriched blood had far better survival times.
Between the two experiments, the researchers suggest that it is reasonable to think that a diet that helps Proteobacteria flourish in the gut could boost IgA-levels, providing protection against sepsis.