Why do we age? What exactly is happening in our bodies? And can we do anything about it? Mankind has sought answers to these questions since time immemorial.
In a new study, researchers have uncovered processes within our immune system that contribute to aging.
They found that low levels of the hormone cortisol and the protein known as GILZ can trigger chronic inflammatory responses in the body and cause aging.
The research was conducted by a team from Saarland University.
The phenomenon of human aging is the result of a complex interaction between numerous factors, with our own immune system playing a critical role. As we get older, our body’s own defense mechanisms age, too.
The adaptive or specific immune system that each of us acquires over the course of our lives and that protects us from the pathogens that we came into contact with gradually deteriorates as we age.
In contrast, however, our innate or non-specific immune system, which is the first line of defense towards a wide variety of pathogens, becomes overactive. The result is chronic inflammation.
A persistent state of inflammation can cause serious damage to our bodies.
One consequence is that chronic inflammatory diseases, such as atherosclerosis or arthritis, are far more prevalent in older patients.
The scientific community refers to this phenomenon as ‘inflamma-aging’—a portmanteau word that combines the two inseparably linked processes of inflammation and aging.
What was uncertain up until now was what actually caused these inflammatory responses to flare up.
In the study, the team provided some important insight.
According to them, the inflammatory process is linked to the fact that the amount of cortisol generated in the body decreases as we get older.
Cortisol and its inactive form cortisone commonly referred to as stress hormones, are released by the adrenal gland.
The hormone cortisol acts as a biochemical signaling molecule and is involved in numerous metabolic processes in the body. Cortisol deficiency in the body leads to an inflammatory response.
The serum level of cortisol in the body is lower in the elderly. Moreover, macrophages, an important type of immune cells, can convert inactive cortisone to active cortisol, but this ability declines with increasing age.
Macrophages are important cells within the immune system that use signaling molecules to control other immune cells. They play a critical role in determining the extent of our body’s inflammatory response.
However, macrophage function becomes impaired with increasing age.
This can lead to an increase in the quantities of pro-inflammatory signaling molecules, which in turn drives the activity of other inflammatory cells of the body’s immune system.
The team found one particular protein is implicated in the malfunctioning of macrophages in the elderly. The protein is known as GILZ and its levels are regulated in part by cortisol.
It plays a critical role in many important processes in the human body. It plays a key role in our immune system, for example, it’s involved in switching off the macrophage inflammatory response.
The study shows that a lower cortisol level causes macrophages to produce less GILZ, which in turn means that the macrophages simply continue to release inflammatory signaling molecules.
The team found that GILZ levels are indeed lower in older people.
To find out whether that in itself was enough to cause an inflammatory response, Hoppstädter genetically deactivated the GILZ protein.
The data showed that the macrophages were activated and there was a resulting increase in chronic inflammatory processes.
The team says a huge amount of work still needs to be done before we have a medically effective drug.
The phenomenon of human aging remains immensely complex, but the work has moved one small step further to a better understanding of why and how people age.
One author of the study is the pharmaceutical scientists Alexandra K. Kiemer.
The study is published in Aging Cell.
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