Research indicates that an excessive intake of salt could wreak havoc with your immune system. Researchers indicate that excess consumption could damage key immune regulators known as regulatory T cells by disrupting their energy metabolism and disrupting their work.
Regulatory T cells regulate immune reactions in an orderly manner. But excessive salt consumption reduces their energy supply, making them temporarily dysfunctional.
Research has demonstrated that an excess of salt in our diets may negatively impact metabolism and energy balance of macrophages and monocytes innate immune cells and hinder them from operating at optimal efficiency.
Salt has long been known to trigger malfunctions in cells’ power plants known as mitochondria, leading to potential malfunctions within adaptive immune cells such as regulatory T cells or Tregs. Researchers wanted to see whether an overdose of salt might also create similar problems with Tregs.
Tregs play an essential part of adaptive immunity, serving to balance normal function with harmful inflammation. Sometimes called the “immune police”, Tregs ensure that immune responses take place safely without impacting on host organisms.
Studies suggest that deregulated Tregs may contribute to autoimmune diseases like multiple sclerosis. Additional research has uncovered problems in Tregs mitochondrial function of patients diagnosed with autoimmunity; yet their exact causes remain unknown.
Based on previous results that salt can influence macrophage and monocyte mitochondrial function as well as recent findings of Tregs from patients with autoimmunity, researchers wanted to ascertain whether similar problems would occur among healthy individuals’ Tregs.
Previous studies have discovered that too much salt could disrupt Treg function by creating an environment similar to an autoimmune condition – this means too much salt makes Treg cells behave similarly to those involved in such illnesses; yet how exactly this hinders their performance remains unknown.
In this study, researchers determined that sodium causes Treg function disruption by altering cell metabolism changes that interfere with mitochondrial energy generation. This mitochondrial issue seems to be at the core of how salt modifies Treg function, leading to gene expression changes similar to those seen in dysfunctional Tregs found in autoimmune conditions.
Even short-term mitochondrial function disruption had long-term ramifications on Treg fitness and immune-regulating ability in different experimental models, suggesting sodium could play an integral part in Treg dysfunction – potentially contributing to various diseases – but further studies are required for verification of this theory.
