Inflammation is a good servant but a bad master. Sadly, the human immune system is quite imperfect and a well-meant inflammation can lead to serious problems. That is why it would be handy to have drugs that can turn inflammation off.
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Inflammation Is Evil
Inflammation is essentially a weapon of the immune system that the body uses against various threats. But it is quite a destructive and hard to control weapon that can often do a lot of collateral damage. A lot of problems are caused by chronic inflammation and inflammation is a major factor in many neurodegenerative diseases, diabetes, and similar systemic diseases.
A team from the University of California, Berkeley recently tracked down a molecular switch in the genes of mice that could cause a storm in medicine. It seems that it is capable of turning of inflammation and also revert its consequences for the surrounding tissue. And because inflammation often comes with aging the molecular switch might be also able to relieve the effects of aging.
To Acetylate Or To Deacetylate
A new study led by Danica Chen is all about a complex called the inflammasome NLRP3. This is a protein oligomer that is made from several enzymes. These complexes are created in myeloid cells and are part of your natural immunity. Their purpose is to activate inflammatory processes and to start pyroptosis – one of the kinds of preprogrammed cellular death. Inflammasomes watch tissues and when they “think” something is weird they start an inflammation.
Under normal circumstances, inflammation is wanted and is a powerful tool for defending the body. But a dangerous tool. The human body has flaws and thus sometimes an inflammation does harm. Chronic inflammation is unpleasant, hurt, and subject the body to a risk of other and larger health complications.
But that could change. Chen and her colleagues found that an enzyme SIRT2 (NAD-dependent deacetylase sirtuin 2) functions as an off switch for inflammation. It is precisely deacetylation that plays a key role in switching an inflammation on and off. When a certain part of the inflammasome NLRP3 is acetylated it is turned on. And when you deacetylate it the inflammasome NLRP3 turns off.
The scientists tested the switch by creating genetically modified mice without the SIRT2 protein. They let them live for two years and then they compared their health with a control group of mice. In the end, it was shown that the mice without SIRT2 have more traces of inflammation and are more resistant to insulin that is closely linked to type 2 diabetes.
The researchers are convinced that now we will be able to develop drugs that will effectively turn off inflammasomes. That should add to our options for treating diabetes, multiple sclerosis, Alzheimer's diseases, Parkinson's disease, and other similar systemic diseases. And another recent research showed that the NLRP3 molecule can also be turned off by the MCC950 molecule.
Drugs that turn off inflammation could become a key part of anti-aging drugs. Chen's team is currently focusing on this and is searching for mechanisms that could allow us to revert the effects of aging. And inflammation will likely play a major role.
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