Consuming Too Much Salt May Trigger Autoimmune Ill
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Consuming too much salt affects an individual’s cardiovascular system and blood pressure negatively while also impacting the immune system adversely. A new study has now found that the consumption of too much salt weakens the energy supply of regulatory T cells, preventing them from working properly.
Regulatory T cells are cells that help maintain homeostasis in the body by suppressing immune responses that may cause excessive inflammation. The study was carried out by a global team of researchers coordinated by researchers at the Max Delbrück Center in Germany, Hasselt University and the VIB Center for Inflammation Research in Belgium.
A couple of years ago, teams of researchers led by Professor Dominik Müller of the Max Delbrück Center for Molecular Medicine and Professor Markus Kleinewietfeld of the VIB Center for Inflammation Research discovered that diets with too much salt negatively impacted the energy balance and metabolism of macrophages and monocytes. The investigators also demonstrated that salt triggers malfunctions in the mitochondria, which generates the chemical energy needed to power cells in the body.
These discoveries are the basis of the new study, which focused on whether excessive intake of salt could create the same problem in regulatory T cells. Researchers believe that regulatory T cell deregulation is associated with the development of autoimmune illnesses such as multiple sclerosis. This latest study was also led by Müller and Kleinewietfeld, with Dr. Ibrahim Hamad and Dr. Beatriz Côrte-Real from the VIB Center for Inflammation Research as first authors.
The researchers found that high sodium intake disrupted how regulatory T cells function by modifying cellular metabolism and interfering with how the mitochondria generated energy. This, the researchers explained, was probably the first step in how sodium altered T cell function and led to changes in gene expression. In their report, the scientists noted that disrupting the function of mitochondria even for a short period had long-lasting consequences on the immune-regulation capacity and fitness of regulatory T cells, as observed in different experimental models.
Kleinewietfield stated that understanding the underlying molecular mechanisms that contributed to dysfunction of regulatory T cells in autoimmunity was important. He added that since these cells played a role in various illnesses, looking into such salt-elicited effects could also provide new strategies for modifying regulatory T cell function in different illnesses.
The study’s findings, which were reported in “Cell Metabolism,” will also afford researchers new avenues for exploring the development of cardiovascular and autoimmune illnesses.
The rising toll of autoimmune conditions has led various for-profit companies, including Aditxt Inc. (NASDAQ: ADTX), to focus on finding ways to retrain people’s immune systems so that the progress of autoimmune diseases can be slowed or even reversed.
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