Artem R. Oganov & Weiwei Zhang
for decades, doctors have been admonishing us to reduce salt to reduce the chances of a heart attack or stroke. Now there may be another reason to avoid seasoning: studies in rodents and cultured cells, reported today, show that dietary salt could promote autoimmune diseases such as multiple sclerosis and inflammatory bowel diseases.
The studies "have done a wonderful job of pushing knowledge forward and explore something that is potentially clinically important," says immunologist David Fox from the University of Michigan Medical School in Ann Arbor, who was not involved in the research. Daniel Cua, an immunologist at Merck Research Laboratories in Palo Alto, California, agrees. The work "is really well done with a lot of mechanistic understanding."
The results suggest that the salt stimulates the specialization of T H 17 cells. Although these immune cells protect us against bacteria and fungi, they have also been implicated in diseases such as inflammatory bowel disease, multiple sclerosis and psoriasis. T H 17 mature cells from non-specialized T cells, and, according to their influences, they can be beneficial or destructive.
The researchers have converged on the results of different directions. Immunobiologist David Hafler of the Yale School of Medicine and colleagues found that people who admitted to eating lots of fast food harbored more T H 17 cells. An ingredient that fast food contains prodigious amounts is salt. To determine whether the salt represented excess T H 17 cells, Hafler and colleagues doped T cell cultures with unskilled sodium chloride. "The results were perhaps the most dramatic of my career as a researcher," he said. Modestly raise salt concentrations, mimicking the levels in the tissues of an animal a diet high in salt, increased the number of T H 17 cells that matured in crops almost 10 times . And these T H 17 cells began to molecules causing inflammation, indicating that they had become the harmful variety.
The scientists then tested whether this effect sinister occurred in animals. They made mice develop encephalomyelitis experimental autoimmune (EAE), a neurological disease similar to multiple sclerosis which is favored by "bad" T H 17 cells. They fed some meals rodents that contained about as much salt as a typical Western diet. Compared to animals that lived on the poor food salt, mice that nibbled chow rich in salt developed EAE earlier and had more severe symptoms, the team reports in Nature .
Working independently of the group Hafler, calculating biologist Aviv Regev of the Broad Institute in Cambridge, Massachusetts; Vijay Kuchroo immunologist at Harvard Medical School in Boston; and colleagues also hit a link between salt and autoimmunity. They tracked gene activity during the period T H 17 cell maturation three days and revealed the molecular circuitry that controls the process. One of the most influential genes of this network was SGK1 , and it has a salt connection, helping cells to manage the levels of sodium. Using T cell cultures, the team found that salt promotes specialization of T H 17 cells SGK1 .
The sodium content is higher in the fluids of the body tissues, where T H 17 cells fight against pathogens in the blood stream. T H The sensitivity of 17 cells salt can be adaptive in normal conditions, ensuring that they rotate in the right place. "You do not want the activated T cells in peripheral blood," said Hafler. "You want them to be activated when they go into the tissues."
But rising salt levels by eating a lot of salty foods could mean trouble. The medical implications of the results could be profound, human genetics notes Judy Cho of the Yale School of Medicine, who was not involved in the research. For example, autoimmune diseases such as multiple sclerosis and type 1 diabetes have become more common in recent decades, "a massive increase in salt intake could easily explain."
Researchers must now confirm that the salt is a factor in human autoimmune diseases, says immunologist John O'Shea from the National Institute of Arthritis and Musculoskeletal and Skin Diseases Bethesda, Maryland. People should not assume that the link is "a done deal" in humans. Scientists are ready to discover Kuchroo said. "The scene is ready to make accurate experiments to test the hypothesis."
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