The new study describes how molecules produced by gut bacteria help control the activity of a protein known to suppress inflammation.

Around 50 years ago, researchers discovered a protein that seemed to play a major role in reducing the efficacy of cancer treatments. Called P-glycoprotein (P-gp), one of its important functions is to catch and pump out foreign substances that enter cells.

This particular role has made P-gp a focus for cancer researchers as it has been found to significantly reduce the effectiveness of chemotherapy. But more recently P-gp has been found to also play a key anti-inflammatory role in the gut, producing molecules known as endocannabinoids which suppress inflammation.

In cases of chronic intestinal inflammation, such as ulcerative colitis, P-gp expression is reduced. And in those cases of intestinal inflammation researchers also detected major imbalances in gut bacteria populations. But before now it hasn't been clear exactly how the microbiome could be influencing P-gp expression.

The new research found P-gp expression is influenced by a combination of gut bacteria metabolites. Most importantly the research found P-gp expression is not regulated by one single metabolite or species of bacteria. Instead, P-gp expression is induced by a synergistic combination of a short-chain fatty acid known as butyrate and three secondary bile acids (LCA, DCA, and UDCA).

Optimal P-gp expression was detected only when all of these molecules were working in concert with one another. Merran Dunford, a researcher from the University of Bath working on the study, says the big finding here is the discovery of a cross-talk mechanism highlighting how a healthy microbiome can communicate with the immune systems to keep inflammatory activity in the gut in balance.