Share This Page

Excess salt, autoimmune diseases linked

| Sunday, March 10, 2013, 5:39 p.m.

CHICAGO — Increased salt consumption may be a key culprit behind rising rates of autoimmune diseases such as multiple sclerosis, researchers reported in a trio of papers looking at the role of a specific class of cells linked with inflammation.

Reporting in the journal Nature, the researchers said high-salt diets increased levels of a type of immune cell linked with autoimmune disease. And mice genetically engineered to develop multiple sclerosis got much worse when they ate what amounted to a high-salt Western diet compared with mice that had more moderate salt intake.

The findings suggest that salt may play a previously unknown role in triggering autoimmune diseases such as MS or type 1 diabetes in individuals who are genetically predisposed.

“It's not bad genes. It's not bad environment. It's a bad interaction between genes and the environment,” said Dr. David Hafler, a professor of immunobiology at Yale University in New Haven, Conn., and senior author of one of the three papers.

High salt intake is a known culprit in increasing the risk of heart disease and hypertension. The new study implicates high-salt diets in increasing rates of autoimmune disease.

“It can't be just salt. We know vitamin D probably plays a small component. We know smoking is a risk factor. This now suggests that salt is also a risk factor,” Hafler said.

“How much? We don't know,” he added.

Hafler became interested in studying the link between salt and autoimmunity through studies of the gut microbiome — a census of gut microbes and cell function of 100 healthy individuals.

The team noticed that when people in the study visited fast-food restaurants more than once a week, they saw a marked increase in levels of destructive inflammatory cells, which the immune system produces to respond to injury or foreign invaders, but which attack healthy tissues in autoimmune diseases.

He shared these findings with colleagues at Harvard Medical School, the Broad Institute of Harvard, the Massachusetts Institute of Technology and others who were working out what factors induce the activity of a type of autoimmune cell known as a T helper 17 or a Th17 cell.

Th17 cells can promote inflammation that is important for defending against pathogens, but they have also been linked to diseases like multiple sclerosis, psoriasis, rheumatoid arthritis, and ankylosing spondylitis. Treatment options for some of these diseases, such as psoriasis, include manipulating T cell function.

“The question we wanted to pursue was: How does this highly pathogenic, pro-inflammatory T cell develop?” said Vijay Kuchroo of the Harvard-affiliated Brigham and Women's Hospital and a member of the Broad Institute.

“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.”

Hafler said Kuchroo's team worked on tracing how these immune cells were wired, and what triggered their development. They identified a specific gene known as SGK1 that plays an important role in the cells' development. This gene had not been seen in T cells before, but it has been known to play a role in absorbing salt in the gut and kidneys.

Researchers at Harvard and Yale and colleagues in Germany led by Dominik Mueller looked to see whether a high-salt diet could induce the destructive immune system response that is the hallmark of autoimmunity.

They found that adding salt to the diet of mice induced the production of Th17 cells and that mice genetically engineered to develop a form of MS had more severe disease than mice fed a normal mouse diet.

Hafler says the findings now need to be studied in people.

It likely will be years before this link is confirmed, but Hafler says for patients at risk of autoimmune disease, reducing dietary salt may be a good idea.

TribLIVE commenting policy

You are solely responsible for your comments and by using TribLive.com you agree to our Terms of Service.

We moderate comments. Our goal is to provide substantive commentary for a general readership. By screening submissions, we provide a space where readers can share intelligent and informed commentary that enhances the quality of our news and information.

While most comments will be posted if they are on-topic and not abusive, moderating decisions are subjective. We will make them as carefully and consistently as we can. Because of the volume of reader comments, we cannot review individual moderation decisions with readers.

We value thoughtful comments representing a range of views that make their point quickly and politely. We make an effort to protect discussions from repeated comments either by the same reader or different readers

We follow the same standards for taste as the daily newspaper. A few things we won't tolerate: personal attacks, obscenity, vulgarity, profanity (including expletives and letters followed by dashes), commercial promotion, impersonations, incoherence, proselytizing and SHOUTING. Don't include URLs to Web sites.

We do not edit comments. They are either approved or deleted. We reserve the right to edit a comment that is quoted or excerpted in an article. In this case, we may fix spelling and punctuation.

We welcome strong opinions and criticism of our work, but we don't want comments to become bogged down with discussions of our policies and we will moderate accordingly.

We appreciate it when readers and people quoted in articles or blog posts point out errors of fact or emphasis and will investigate all assertions. But these suggestions should be sent via e-mail. To avoid distracting other readers, we won't publish comments that suggest a correction. Instead, corrections will be made in a blog post or in an article.