ISLAMABAD: Now, researchers at Washington University School of Medicine in St. Louis have found that a kind of tolerance-promoting immune cell appears in mice that carry a specific bacterium in their guts. Further, the bacterium ¬needs tryptophan - one of the building blocks of proteins - to trigger the cells' appearance.
"We established a link between one bacterial species - Lactobacillus reuteri - that is a normal part of the gut microbiome, and the development of a population of cells that promote tolerance," said Marco Colonna, MD, the Robert Rock Belliveau MD Professor of Pathology and the study's senior author. "The more tryptophan the mice had in their diet, the more of these immune cells they had."
If such findings hold true for people, it would suggest that the combination of L. reuteri and a tryptophan-rich diet may foster a more tolerant, less inflammatory gut environment, which could mean relief for the million or more Americans living with the abdominal pain and diarrhea of inflammatory bowel disease.Cervantes-Barragan collaborated with Chyi-Song Hsieh, MD, PhD, the Alan A. and Edith L. Wolff Distinguished Professor of Medicine, to sequence DNA from the intestines of the two groups of mice. They found six bacterial species present in the mice with the immune cells but absent from the mice without them.
To understand how the bacteria affected the immune system, the researchers grew L. reuteri in liquid and then transferred small amounts of the liquid - without bacteria - to immature immune cells isolated from mice. The immune cells developed into the tolerance-promoting cells. When the active component was purified from the liquid, it turned out to be a byproduct of tryptophan metabolism known as indole-3-lactic acid.
Tryptophan - commonly associated with turkey - is a normal part of the mouse and the human diet. Protein-rich foods contain appreciable amounts: nuts, eggs, seeds, beans, poultry, yogurt, cheese, even chocolate.
When the researchers doubled the amount of tryptophan in the mice's feed, the number of such cells rose by about 50 percent. When tryptophan levels were halved, the number of cells dropped by half.
People have the same tolerance-promoting cells as mice, and most of us shelter L. reuteri in our gastrointestinal tracts. It is not known whether tryptophan byproducts from L. reuteri induce the cells to develop in people as they do in mice, but defects in genes related to tryptophan have been found in people with inflammatory bowel disease.
"The development of these cells is probably something we want to encourage since these cells control inflammation on the inner surface of the intestines," Cervantes-Barragan said. "Potentially, high levels of tryptophan in the presence of L. reuteri may induce expansion of this population."