Researchers have begun to paint a picture of how one common ingredient can cause disorders in the immune system, like diabetes and multiple sclerosis.
That ingredient is salt. But not just any salt, the salt in processed foods.
Autoimmune disease is generally caused when the immune system, which protects us from foreign pathogens, accidentally begins to attack the body’s natural, normal tissues. Autoimmune diseases include tape 1 diabetes, IBS, and MS. There are potentially genetic causes of these diseases, but a number of environmental factors can lead to these diseases too.
Immune cells called T helper 17 (Th17) cells help us fight infection, but they’ve also been linked with several autoimmune disorders. Th17 cells, along with other types of helper T cells, arise from naive T cells. Researchers had identified specific factors that induce the development of Th17 cells, but the downstream factors that guide and control the cells’ development were largely unknown.
Several research groups—at Yale University, the Broad Institute, Harvard University, MIT, Brigham and Women’s Hospital, and others—have been exploring the development of Th17 cells. Their work has been funded by several NIH components, including the National Institute of Allergy and Infectious Diseases (NIAID), National Institute of Neurological Disorders and Stroke (NINDS) and National Human Genome Research Institute (NHGRI). A trio of new papers describing their findings was published online in Nature on March 6, 2013.
A team led by Dr. Aviv Regev studied genes expressed at different time points during Th17 cell development. Computer modeling helped to identify 3 major waves of gene expression over time. They detected almost 1,300 genes involved in over 10,000 interactions, with 71 regulators. Using silicon nanowires to deliver short interfering RNA (siRNA) into naive T cells, the researchers were able to interfere with the expression of specific genes to further validate the internal network used to build Th17 cells. They validated 39 of the regulatory factors with this new technique.
Using information from the network analysis, a related team led by Dr. Vijay K. Kuchroo studied gene expression in developing Th17 cells after activation of a receptor that involves the cells in autoimmunity. They identified a key protein in the cell’s development called serum glucocorticoid kinase 1 (SGK1). To test its role in autoimmune disease, they examined a mouse disease that resembles human multiple sclerosis. Mice lacking SGK1 had less severe symptoms and significantly reduced rates of the disease, known as experimental autoimmune encephalomyelitis (EAE).
A third study also found that mice and human T cells when exposed to increased sodium levels turned to Th17 cells. These mice on high salt diets often developed more severe forms of EAE.
“It’s premature to say, ‘You shouldn’t eat salt because you’ll get an autoimmune disease.’” Regev says. “We’re putting forth an interesting hypothesis—a connection between salt and autoimmunity—that now must be tested through careful epidemiological studies in humans.”
“Once we have a more nuanced understanding of the development of the pathogenic Th17 cells, we may be able to pursue ways to regulate them or their function,” Kuchroo adds.
So it’s not to say that you should just cut out sodium entirely. These are preliminary studies. One thing is for sure: most Americans do consume too much salt, and it may be time to consider how much salt is in your diet and what you can do to reduce it if you’re taking in too much.
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