According to research, consuming an excessive amount of salt could affect the immune system adversely. The researchers report that excess salt consumption can disrupt important immune regulators known as regulatory T cells by harming their energy metabolism.
Regulatory T cells make sure that immune responses take place in a controlled manner. But consuming excess salt weakens the energy supply of these cells, subsequently rendering them temporarily dysfunctional.
Previous research has revealed that excess salt in the diet can impact the metabolism and energy balance adversely in certain kinds of innate immune cells known as macrophages and monocytes and prevent them from functioning properly.
It has also been shown that salt activates malfunctions in the power plants of the cells known as the mitochondria. For the current study, the researchers wanted to find out if too much salt could also produce a similar issue in adaptive immune cells such as regulatory T cells, also called Tregs
Tregs play an important role in the adaptive immune system. They’re in charge of balancing normal function with harmful excess inflammation. They are at times called the “immune police” as they make sure that immune responses take place in a controlled way without the host organism being harmed.
It’s believed that Tregs deregulation is associated with autoimmune diseases such as multiple sclerosis. Other studies have identified problems in the Tregs mitochondrial function of autoimmune patients, although the contributing factors are unknown.
Considering the previous results of salt influencing the macrophage and monocyte mitochondrial function together with the new findings on mitochondria in Tregs from patients with autoimmunity, the researchers wanted to find out if sodium would result in similar problems in Tregs of healthy individuals.
Previous studies have also found that too much salt could influence Treg function by producing an autoimmune-like environment. This means that excess salt makes the Treg cells resemble those involved in autoimmune disorders. Just how salt impairs Treg function hadn’t however yet been discovered.
The current study found that Treg function is disrupted by sodium from cellular metabolism changes by interfering with the generation of mitochondrial energy. This mitochondrial issue appears to be the initial phase in the way Treg function is modified by salt, resulting in gene expression changes that exhibited similarities to those in autoimmune condition Tregs that are dysfunctional.
Even a short-term mitochondrial function disruption had long-term implications for the fitness and immune-regulating ability of Tregs in different experimental models. These results indicate that sodium could be a factor that could play a role in Treg dysfunction, potentially contributing to various diseases, but this must be confirmed in more research.
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