Interleukin 1-beta, or IL-1β, a protein produced by white blood cells, promotes your body’s production of insulin in response to eating. Together, IL-1β and insulin activate your body’s immune response and enhance its ability to utilize glucose, according to a new report published in the journal Nature Immunology (paywall).
If you’ve ever endured the fallout from a bad dietary decision at your local food truck, then you’ve experienced first hand how your body maintains the delicate balance between acquiring the necessary calories and nutrients for your day-to-day existence and simultaneously protecting you from serious, sometimes deadly, infection.
Every time you eat, you ingest bacteria – fellow travelers that hitch rides on your food.
Fortunately, your body has a defense mechanism that rivals most nations’ early tactical response teams – the innate immune system, a collection of cells and proteins always on alert and ready to respond to foreign attack. The end result of immune system activation is inflammation.
Some research suggests that eating is associated with mild, short-lived inflammation. The principal activator of this inflammation is IL-1β, a tiny protein produced by white blood cells called macrophages.
In a recent study, researchers at the University Hospital Basel in Switzerland hypothesized that IL-1β not only drives post-meal immune system activation and inflammation, it also promotes the production of insulin, which helps your body utilize glucose. Why? To fuel the immune cells actively engaged in containing the bacteria in the foods you eat.
Using an animal model with ordinary (“wild type”) mice, the researchers discovered that the number of macrophages in the guts of the wild type mice increased after feeding. In turn, the macrophages produced IL-1β, which led to immune system activation and an increase in insulin production. The insulin bolstered the inflammatory response by stimulating the macrophages to produce more IL-1β.
They also discovered that the macrophages in the wild type mice only produced IL-1β if they had been exposed to bacteria and if their blood glucose was elevated due to eating.
The researchers noted that although IL-1β and insulin worked together to help the mice utilize glucose, IL-1β favored the immune cells – increasing their ability to take in more glucose (compared to other cells).
Activation of the innate immune system is important for our survival. But eating too much can cause prolonged activation, eventually leading to the development of metabolic disorders, such as diabetes, gout, and cardiovascular disease. And, in a strange paradox, IL-1β is both beneficial and toxic to certain cells in the pancreas. Short-term exposure to IL-1β helps the pancreatic cells regenerate, but long-term exposure to IL-1β destroys the cells.
This synergistic cooperation between your immune system and your gut is what keeps you healthy and well fed.
Dror, E., Dalmas, E., Meier, D. T., Wueest, S., Thévenet, J., Thienel, C., … & Item, F. (2017). Postprandial macrophage-derived IL-1 [beta] stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nature Immunology.