WEDNESDAY, March 6 (HealthDay News) -- Eating lots of foods loaded with salt may do more than raise your blood pressure: Researchers report that it could also contribute to the development of autoimmune diseases, where the body's immune system mistakenly mounts an attack upon some part of the body.

A significant increase in the incidence of autoimmune diseases, especially multiple sclerosis and
type 1 diabetes, suggests that environmental factors, and not genetics, may explain the trend, the researchers noted.

"The diet does affect the autoimmune system in ways that have not been previously recognized," said senior study author Dr. David Hafler, a professor of neurology and immunobiology at the Yale School of Medicine, in New Haven, Conn.

It was an accidental discovery that triggered the researchers' interest in salt; they stumbled upon the fact that people who ate at fast food restaurants seemed to have higher levels of inflammatory cells than others, Hafler explained.

In the study, Hafler and his team found that giving mice a high-salt diet caused the rodents to produce a type of infection-fighting cell that is closely associated with autoimmune diseases. The mice on salt diets developed a severe form of multiple sclerosis, called autoimmune encephalomyelitis. Findings from animal studies are not always mirrored in human trials, however.

Inflammatory cells are normally used by the immune system to protect people from bacterial, viral, fungal and parasitic infections. But, in the case of autoimmune diseases, they attack healthy tissue.

Hafler's study is one of three papers, published in the March 6 issue of the journal Nature, that show how salt may overstimulate the immune system. In addition to Hafler's research, scientists from the Broad Institute in Boston explored how genes regulate the immune response, and researchers from Harvard Medical School and Brigham and Women's Hospital in Boston zeroed in on how autoimmunity is controlled by a network of genes.

All three studies help explain, each from a different angle, how "helper" T-cells can drive autoimmune diseases by creating inflammation. Salt seems to cause enzymes to stimulate the creation of the helper T-cells, escalating the immune response.

"We think of helper T-cells as sort of the orchestra leaders, helping the immune system know what the cells should be doing in response to different microbial pathogens," explained Dr. John O'Shea, director of intramural research at the U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases, in Bethesda, Md. "The strength of these papers is that they have found another factor that drives [helper T-cell] differentiation -- salt."

While salt may play a role in autoimmune diseases, the researchers said the picture is most likely complicated. "We don't think salt is the whole story. It's a new, unexplored part of it, but there are hundreds of genetic variants involved in autoimmune disease and environmental factors, too," said Hafler.

It's also unclear just how much salt is required to stimulate the autoimmune response, Hafler added.

In addition to salt, other factors have been shown to influence levels of helper T-cells, including microbes, diet, metabolism, environmental factors and cytokines (proteins that help regulate inflammatory responses), according to O'Shea, who was not involved with the new studies.

O'Shea said the studies provide a way to test -- hopefully soon in human trials -- whether a low-salt diet might help treat autoimmune disease.

"They have now identified a biomarker, so you could treat people with a low-salt diet and then check for the marker in cells using cell cytometry, for example," O'Shea explained. While such a test is not generally available for consumers, it is found in most research labs, he added.

Hafler pointed out that while salt may be implicated in autoimmune disease, it may also be found to play an important role in boosting the immune system. Part of the reason chicken soup seems to be effective with
colds and flu may be that the salt stimulates an infection-fighting response, he said.

Should consumers who are concerned about autoimmune disease switch to a low-salt diet, even before tests in humans have been done?

"If I had an autoimmune disease, I would put myself on a low-salt diet now," Hafler said. "It's not a bad thing to do. But we have to do more studies to prove it."

O'Shea agreed. "But the extent to which salt is important, I think we don't know. These papers show it experimentally, but we still can't be sure," he said.

SOURCES: David Hafler, M.D., professor, neurology and immunobiology, and chair, department of neurology, Yale School of Medicine, New Haven, Conn.; John O'Shea, M.D., director, intramural research program, U.S. National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, Md.; March 6, 2013, Nature