Recent research indicates that both animals and humans have intricate interactions with bacteria within and around them. The gut microbiome in humans has been linked to conditions like depression and Parkinson\u2019s disease. A study by neuroscientists from The Picower Institute for Learning and Memory at MIT aims to understand how the bacterial microbiome affects brain function, using the nematode Caenorhabditis elegans as a model.<\/p>\n
The study, published in Current Biology and led by Picower Fellow Cassi Estrem in the lab of Associate Professor Steven Flavell, explores the specific chemicals a key neuron in C. elegans detects in both beneficial and harmful bacteria. Flavell, an investigator at the Howard Hughes Medical Institute and MIT faculty member, highlights the significant impact of bacterial cells, which outnumber human cells, on health. The research seeks to uncover the mechanisms by which bacteria in the gut influence the host nervous system.<\/p>\n
Understanding these interactions could advance therapeutic interventions, says Flavell. C. elegans, described as a “bacterial specialist,” has evolved to consume bacteria while avoiding harmful types. The lab previously found that the NSM neuron in the worm uses “acid sensing ion channels” (ASICs) to detect ingested bacteria, releasing serotonin to increase feeding and slow movement.<\/p>\n
To pinpoint what the ion channels detect, the team tested 20 bacterial types, identifying polysaccharide sugars as the activators of NSM. In gram-positive bacteria, peptidoglycan was the trigger, while a different polysaccharide affected gram-negative bacteria. Experiments showed polysaccharides and peptidoglycan promote feeding behavior, and disrupting ASICs eliminated these responses.<\/p>\n
The researchers also investigated how worms identify harmful bacteria, using Serratia marcescens, a bacterium harmful to humans. Red strains, containing prodigiosin, were highly lethal. When prodigiosin was present, NSM did not activate, preventing ingestion. Adding prodigiosin to benign bacteria suppressed NSM activity, demonstrating an evolved avoidance of danger-associated chemicals.<\/p>\n
Flavell suggests these mechanisms may be relevant to other animals, noting the molecular components identified are present across species, including mammals. “We developed a method for identifying these pathways in a bacterial detection specialist,” he says. The study, supported by several foundations and the NIH, included authors Malvika Dua, Colby Fees, Greg Hoeprich, Matthew Au, Bruce Goode, and Lingyi Deng.<\/p>\n