Friday, 17 March 2017

Gut inflammation controlled by changing bacterial balance


Numerous human diseases, including inflammatory bowel disease, diabetes and autism spectrum disorders have been linked to abnormal gut microbial communities, or microbiomes, but an open question is whether these altered microbiomes are drivers of disease.
A new study at the University of Oregon, led by postdoctoral fellow Annah Rolig, took aim at that question with experiments in zebrafish to dissect whether changes in the abundance of certain gut bacteria can cause intestinal inflammation.

The researchers successfully tracked how gut bacterial abundances influenced inflammation. Fish with intestinal inflammation had a larger abundance of a subset of bacteria that appeared to be pro-inflammatory, which they confirmed by dosing the fish with one of these bacteria and finding that it increased the severity of disease symptoms.

They also found a subset of bacteria that was depleted in the inflamed intestines, but present in the mutant fish that remained disease-free. Dosing the fish with a strain of these depleted bacteria ameliorated the disease. Finally, they showed that they could cure the inflammation by transplanting gut neurons from healthy fish into the diseased fish.

These studies demonstrate that inflammatory intestinal pathologies, such as Hirschsprung-associated enterocolitis or inflammatory bowel disease, can be explained as an overgrowth of certain pro-inflammatory groups of bacteria or a loss of anti-inflammatory bacteria, said Judith Eisen, a professor of biology and an expert on gut neurons in zebrafish.

Identifying the bacteria that drive and protect against disease is the first step toward developing microbial interventions and therapies.

For further details see:

Annah S. Rolig, Erika K. Mittge, Julia Ganz, Josh V. Troll, Ellie Melancon, Travis J. Wiles, Kristin Alligood, W. Zac Stephens, Judith S. Eisen, Karen Guillemin. The enteric nervous system promotes intestinal health by constraining microbiota composition. PLOS Biology, February 2017 DOI: 10.1371/journal.pbio.2000689

Posted by Dr. Tim Sandle

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