Every time you eat, you are inflaming your stomach. And that’s not necessarily a bad thing.

Researchers from the University of Basel in Switzerland found a short-term inflammatory response takes place in your body when you eat, with more immune cells called microphages appearing around your intestines. According to a university statement, depending on how much sugar is in your blood those immune cells will work with insulin, the hormone that controls blood sugar levels, to keep your glucose balanced. This process, mediated by a protein called Interleukin-1beta that carries messages around your body, plays “an important role in sugar uptake and the activation of the immune system.” Because the glucose helps power the immune system, that activation and sugar uptake also protects the body from foreign invaders like bacteria that may be consumed with your meal.

Read: What Is Diabetic Ketoacidosis?

The report was published in Nature Immunology and has implications for people with diabetes. Those patients do not make enough insulin, and therefore cannot adequately control the amount of sugar in their blood, according to the Mayo Clinic. The university says type 2 diabetes comes with chronic inflammation, and there have been clinical studies that aimed to treat the condition by stemming how much of that messenger protein Interleukin-1beta is overproduced in a diabetes patient.

“In diabetes patients, this messenger substance triggers chronic inflammation and causes insulin-producing beta cells to die off,” the statement said.

According to the university, the information may also tell experts why people are more likely to contract an infectious disease during a famine: the body does not get enough nutrients, so rather than sending the little energy it receives to the immune system, it uses that energy on the most critical functions. That leaves the body vulnerable to infection.

Source: Donath MY, Dror E, Dalmas E, et al. Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation. Nature Immunology. 2017.

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