A new study has revealed how the gut's protective mechanisms ramp up significantly with food intake, and at times of the day when mealtimes are anticipated based on regular eating habits.
Researchers from the Walter and Eliza Hall Institute found, in laboratory models, that eating sets off a hormonal 'chain reaction' in the gut.
Eating causes a hormone called VIP to kickstart the activity of immune cells in response to potentially incoming pathogens or 'bad' bacteria. The researchers also found that immunity increased at anticipated mealtimes indicating that maintaining regular eating patterns could be more important than previously thought.
With the rise in conditions associated with chronic inflammation in the gut, such as irritable bowel and Crohn's disease, a better understanding of the early protective mechanisms governing gut health could help researchers to develop prevention strategies against unwanted inflammation and disease.
The research, led by Professor Gabrielle Belz and Dr Cyril Seillet from the Walter and Eliza Hall Institute, was published in the journal Nature Immunology . At a glance
Eating activates immune cells in the gut that protect against pathogens and preserve gut health.
Immunity in the gut also ramps up at regular mealtimes in anticipation of eating and a potentially increased risk of infection.
Understanding the complex interactions between eating, gut health and inflammation could aid in the development of prevention and treatment strategies for chronic inflammatory diseases. Armed against invaders
So how does it work?
When food is consumed nerves in the intestine produce a hormone called vasoactive intestinal peptide (VIP) to 'switch on' a protective response in the gut.
Professor Belz said the team showed, for the first time, that food-induced activation of VIP in preclinical models was vital for a subset of immune cells called ILC3s to mount a protective response in the gut.
Food intake 'switches on' VIP, which plays a critical role in alerting the gut's army of ILC3 immune cells. In response, ILC3s secrete interleukin-22 (IL-22), which swings into protective action to defend against pathogens and maintain tissue integrity.
We also showed that a deficiency in VIP limits the production of IL-22, which in turn negatively impacts the immune system's ability to prevent unwanted inflammation." Professor Gabrielle Belz, Walter and Eliza Hall Institute Related Stories
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