LivingThey discover a molecular "switch" that stops chronic inflammation

They discover a molecular "switch" that stops chronic inflammation

Did you know that chronic inflammation can lead to cancer? As published by the National Cancer Institute of the United States (NCI), chronic inflammation can be caused by infections that do not finish healing, by abnormal reactions of the immune system and even obesity. Over time, chronic inflammation can damage the DNA of cells and cause cancer . The NCI gives an example of patients with chronic inflammatory bowel diseases, such as ulcerative colitis or Crohn’s disease, who are at increased risk of colon cancer.

Chronic inflammation can also occur as a result of old age, stress, and environmental toxins, which cause the immune system to become overloaded.

Now a team of researchers at the University of California, Berkeley, has identified a molecular “switch” that controls the immune machinery responsible for chronic inflammation in the body .

The study’s lead author, Danica Chen, now wonders to what extent aging could be reversed by taking into account inflammation and insulin resistance, conditions that have been associated with degeneration and age-related diseases.

Our immune system has cells called NLRP3 inflammasomes , which are responsible for detecting potential threats to the body and launching an inflammatory response. This is so because when an inflammatory process occurs, white blood cells produce substances that make cells divide and grow to rebuild damaged tissue and repair the injury. Once the wound heals, the inflammatory process normally ends .

However, over-activation of NLRP3 inflammasomes has been linked to chronic diseases such as diabetes, multiple sclerosis, cancer, and dementia.

The good news is that Chen’s team has discovered that they can be deactivated with medication by removing a small piece of molecular matter in a process called deacetylation . This means that it could help prevent chronic diseases or at least treat them. Also the degeneration of the body that occurs as we get older.

“This acetylation can serve as a switch,” Chen said. “So when it’s acetylated, this inflammasome turns on. When it’s deacetylated, the inflammasome turns off.”

The study, which has been published in Cell Metabolism , was carried out in mice reared with a genetic mutation that made them not produce the SIRT2 protein, responsible for deactivating the NLRP3 inflammasome, and normal mice. Well, genetically modified animals showed more signs of inflammation when they reached two years, an advanced age for them, than normal ones. They also experienced increased insulin resistance, which is related to type 2 diabetes and metabolic syndrome.

In addition, the researchers studied adult mice whose immune systems had been destroyed with radiation and then rebuilt with blood stem cells that produced the deacetylated or acetylated version of the NLRP3 inflammasome. Those who received the deacetylated or “quenched” version of the inflammasome improved insulin resistance after six weeks, indicating that turning off this immune machinery could reverse the course of metabolic disease.

“I think this finding has very important implications in the treatment of major human chronic diseases ,” Chen said. “Many promising trials on Alzheimer’s have failed. One possible explanation is that treatment begins too late. Therefore, I think it is more urgent than ever to understand the reversibility of aging-related conditions and use that knowledge to aid development. of a drug for diseases related to aging “.

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