Inflammation is a natural defense used by the body to protect itself. When we get a cut, infection, or injury, the immune system quickly reacts.
It sends special cells and signals to the damaged area to fight germs and help the body heal. This short-term inflammation is useful and necessary for survival.
But sometimes inflammation does not stop when it should. Instead of disappearing after the body heals, the immune system stays active for months or even years. This is called chronic inflammation. Unlike normal inflammation, chronic inflammation slowly damages healthy tissues and organs.
Over time, this constant immune response can increase the risk of many serious illnesses. Scientists believe chronic inflammation plays a role in diseases such as Alzheimer’s disease, Parkinson’s disease, type 2 diabetes, heart disease, and some types of cancer. It is also linked to many problems that appear as people grow older.
Researchers have found that several factors may cause the body to stay in this long-lasting inflammatory state. Aging is one of the most important reasons. As people get older, the immune system sometimes becomes less balanced and more easily triggered.
Long-term stress can also keep the immune system in a constant state of alert. Environmental factors such as air pollution, chemicals, and unhealthy diets may also contribute.
When these factors are present, the immune system may continue reacting even when there is no real threat. Instead of protecting the body, it begins to harm it by damaging healthy cells.
Now, scientists from the University of California, Berkeley have discovered an important clue that may help control this harmful process. The research was led by Professor Danica Chen and was published in the scientific journal Cell Metabolism.
The team identified what they describe as a kind of “switch” inside the immune system that can control chronic inflammation.
At the center of this discovery is a group of immune proteins known as the NLRP3 inflammasome. These proteins act like alarm systems inside immune cells. When they detect danger, such as infection or cell damage, they trigger inflammation to help defend the body.
Normally, this system turns on when needed and then switches off after the danger has passed. However, in many diseases the NLRP3 inflammasome becomes too active and fails to shut down properly. When this happens, it keeps producing inflammatory signals, which can lead to long-term damage throughout the body.
The Berkeley researchers discovered that this system can be turned off through a natural process called deacetylation. This process removes a small chemical piece from the inflammasome protein. When this piece is removed, the inflammasome becomes inactive and stops sending inflammatory signals.
The removal process is controlled by another protein called SIRT2. When SIRT2 performs this action, it essentially turns off the inflammasome and prevents unnecessary inflammation.
To understand how important this mechanism is, the scientists performed experiments using mice. They found that mice that did not have the SIRT2 protein developed much higher levels of inflammation as they aged.
By the time these mice reached two years of age, which is considered old for a mouse, they showed strong signs of chronic inflammation. They also developed insulin resistance. Insulin resistance is a condition in which the body has trouble controlling blood sugar, and it is an early warning sign of type 2 diabetes and other metabolic diseases.
In another experiment, the researchers replaced the immune systems of older mice with new ones created from blood stem cells. These stem cells were specially designed to produce either an active or inactive form of the NLRP3 inflammasome.
The results were striking. Mice that received the inactive version of the inflammasome showed much better insulin sensitivity within only six weeks. This means their bodies were better able to control sugar levels in the blood.
The findings suggest that turning off the inflammasome may not only prevent harmful inflammation but could also help reverse some age-related metabolic problems.
This discovery could have a very large impact on medicine in the future. If scientists can design safe drugs that control this molecular switch, doctors may be able to treat or even prevent diseases caused by chronic inflammation.
Conditions like Alzheimer’s disease and diabetes are often difficult to treat once they have progressed. Some experts believe treatments may fail because they are started too late. If chronic inflammation plays a key role in these diseases, controlling it earlier might greatly improve outcomes.
The study also highlights how closely our lifestyle is connected to our immune system. Diet, stress levels, sleep, and environmental exposures all influence how the immune system behaves.
Many scientists now believe that preventing chronic inflammation may be one of the most important ways to support healthy aging. As researchers continue studying this immune “switch,” they hope to develop new treatments that help people live longer, healthier lives.
If you care about brain health, please read studies about inflammation that may actually slow down cognitive decline in older people, and low vitamin D may speed up cognitive decline.
For more health information, please see recent studies about common exercises that could protect against cognitive decline, and results showing this MIND diet may protect your cognitive function, prevent dementia.
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