Salt May Boost Immune Diseases Through Inflammation
Diets high in salt, tied to hypertension and heart risk in some studies, may also worsen diseases caused by abnormal immune response, laboratory research suggests.
In a study published today in the journal Nature, mice fed high-salt diets had a more severe version of an animal form of multiple sclerosis, an autoimmune disease that affects the central nervous system. Two other papers showed how the cells interact with the body to promote inflammation.
Autoimmune diseases, illnesses such as psoriasis and asthma in which the system that protects the body from invaders wrongly attacks healthy cells, affect as many as 23.5 million in the U.S., according to the National Institutes of Health. The prevalence is rising, though it isn’t clear why. Scientists have suggested genes and the environment play a role.
“It’s very clear in experimental models in animals that there’s a dramatic effect going from low salt to high salt,” said David Hafler, chairman of the department of neurology at Yale School of Medicine in New Haven, Connecticut, and author of one of the studies. The next step is to investigate low-salt diet in people, he said.
Some of the original hints about salt’s role in autoimmune disease were from an observation that eating at fast-food restaurants more than once a week prompted an increase in inflammation, Hafler said.
In human-cell culture, the researchers found that the addition of salt influences the development of certain kinds of T cells, white blood cells that ordinarily help the body fight infections. Some of these cells, called T helper 17, help the gut to maintain the barrier between it and the rest of the body. They also produce an inflammatory cytokine called interleukin-17, which is known to play a role in some autoimmune diseases. Hafler’s group found that in human cells in the lab, adding saline to the cell culture also promoted inflammation.
In a second study, scientists led by Aviv Regev and Vijay Kuchroo from the Broad Institute of MIT and Harvard University, based in Cambridge, Massachusetts, examined these cells further. A third study, also led by Regev and Kuchroo, showed that a salt-sensing enzyme called SGK1 plays a role in creating the harmful reactions from T helper 17 cells.
Other factors besides salt may influence the same pathway, John O’Shea, the scientific director of the National Institutes of Arthritis and Musculoskeletal and Skin Diseases, said in a telephone interview. Though a diet high in salt might worsen autoimmune disease, today’s studies don’t establish exactly which cells the salt works on.
What’s more, autoimmune diseases vary, O’Shea said. Blocking interleukin-17 helps people with psoriasis, while those with inflammatory bowel disease don’t benefit as much. And though the scientists showed that salt worsens disease in mice, the illness was induced by scientists. That may not mean that dietary salt prompts or aggravates spontaneously arising diseases, he said.
“People will be interested in trying to attack these problems,” he said. “One obvious and immediate thing is to look closer at the epidemiology of those autoimmune diseases and see if there really is a link with a high-salt diet. As soon as these papers come out, this is something epidemiologists might be thinking about.”
In some diseases, it might be worthwhile to put patients on a low-salt diet, since it is likely low-risk, O’Shea said. Then scientists could measure the levels of interleukin-17 to see if the levels of inflammation are lower. The natural diseases to start with are psoriasis, allergies and asthma, he said.
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