Chronic inflammation, which results when old age, stress, or environmental toxins keep the body’s immune system in overdrive, can contribute to a variety of devastating diseases, from Alzheimer’s and Parkinson’s to diabetes and cancer.
In a recent study from the University of California Berkeley, scientists found a molecular “switch” that controls the immune machinery responsible for chronic inflammation in the body.
The finding could lead to new ways to halt or even reverse many of these age-related conditions.
In the study, the team found that a bulky collection of immune proteins called the NLRP3 inflammasome—responsible for sensing potential threats to the body and launching an inflammation response—can be essentially switched off by removing a small bit of molecular matter in a process called deacetylation.
Overactivation of the NLRP3 inflammasome has been linked to a variety of chronic conditions, including multiple sclerosis, cancer, diabetes, and dementia.
The results suggest that drugs targeted toward deacetylating or switching off, this NLRP3 inflammasome might help prevent or treat these conditions and possibly age-related degeneration in general.
By studying mice and immune cells, the team found that a protein called SIRT2 is responsible for deacetylating the NLRP3 inflammasome.
Mice that were bred with a genetic mutation that prevented them from producing SIRT2 showed more signs of inflammation at the ripe old age of two than their normal counterparts.
These mice also exhibited higher insulin resistance, a condition linked to type 2 diabetes and metabolic syndrome.
The team also studied older mice whose immune systems had been destroyed with radiation and then reconstituted with blood stem cells that produced either the deacetylated or the acetylated version of the NLRP3 inflammasome.
Those who were given the deacetylated, or “off,” version of the inflammasome had improved insulin resistance after six weeks, indicating that switching off this immune machinery might actually reverse the course of metabolic disease.
The team says the findings have very important implications in treating major human chronic diseases.
It’s also a timely question to ask because, in the past year, many promising Alzheimer’s disease trials ended in failure. One possible explanation is that treatment starts too late, and it has gone to the point of no return.
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The research was published in the journal Cell Metabolism and was conducted by Danica Chen et al.
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