Individuals who consume a diet heavy is salt may increase their risk for a variety of autoimmune diseases, such as multiple sclerosis (MS), according to three new papers published in the journal Nature.
Researchers at Yale Medical School, Harvard Medical School and the Broad Institute have identified dietary salt as the prime suspect in the mystery surrounding the rise the incidence of autoimmune diseases. In accompanying papers in the same issue of Nature, researchers from Brigham and Women’s Hospital and Harvard identified the key molecular pathway involved in the response to salt, and the Broad Institute sketched out the regulatory network of genes that governs this autoimmune response.
“These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment," said Dr. David Hafler, the Gilbert H. Glaser Professor of Neurology, professor of immunobiology, chair of the department of neurology, and senior author of the Yale paper.
The research was inspired, in part, by an observation that eating at fast-food restaurants tended to trigger an increase in production of inflammatory cells, which are mobilized by the immune system to respond to injury or pathogens but which, in autoimmune diseases, attack healthy tissue.
Researchers at Yale and colleagues in Germany led by Dominik Mueller wanted to know whether high salt content in diet might induce the destructive immune system response that is the hallmark of autoimmunity.
They found that adding salt to the diet of mice induced production of a type of T cells previously associated with autoimmune diseases and that mice on salt diets developed a more severe form of an MS animal model, experimental autoimmune encephalomyelitis.
The research at the Broad Institute, Brigham and Women’s Hospital, Harvard University, and Yale University expands the understanding of how one type of immune cell—known as a T helper 17 or Th17 cell—develops, and how its growth influences the development of other kinds of cells involved in the immune system. Reconstruction of this molecular circuitry confirmed the surprising role of salt, the researchers said.
“Humans were genetically selected for conditions in sub-Saharan Africa, where there was no salt," Hafler said. “Today, Western diets all have high salt content and that has led to increase in hypertension and perhaps autoimmune disease as well."
He noted all test-tube cell biology is performed based on the salt levels found in blood and not in the tissues where immune cell ultimately travel to fight infections. That may have been a reason salt’s role in autoimmunity has gone undetected.
“We may have been using the wrong concentrations of salt in our experiments for the past half-century," Hafler said. “Nature did not want immune cells to become turned on in the pipeline, so perhaps blood salt levels are inhibitory."
Researchers at Yale Medical School, Harvard Medical School and the Broad Institute have identified dietary salt as the prime suspect in the mystery surrounding the rise the incidence of autoimmune diseases. In accompanying papers in the same issue of Nature, researchers from Brigham and Women’s Hospital and Harvard identified the key molecular pathway involved in the response to salt, and the Broad Institute sketched out the regulatory network of genes that governs this autoimmune response.
“These are not diseases of bad genes alone or diseases caused by the environment, but diseases of a bad interaction between genes and the environment," said Dr. David Hafler, the Gilbert H. Glaser Professor of Neurology, professor of immunobiology, chair of the department of neurology, and senior author of the Yale paper.
The research was inspired, in part, by an observation that eating at fast-food restaurants tended to trigger an increase in production of inflammatory cells, which are mobilized by the immune system to respond to injury or pathogens but which, in autoimmune diseases, attack healthy tissue.
Researchers at Yale and colleagues in Germany led by Dominik Mueller wanted to know whether high salt content in diet might induce the destructive immune system response that is the hallmark of autoimmunity.
They found that adding salt to the diet of mice induced production of a type of T cells previously associated with autoimmune diseases and that mice on salt diets developed a more severe form of an MS animal model, experimental autoimmune encephalomyelitis.
The research at the Broad Institute, Brigham and Women’s Hospital, Harvard University, and Yale University expands the understanding of how one type of immune cell—known as a T helper 17 or Th17 cell—develops, and how its growth influences the development of other kinds of cells involved in the immune system. Reconstruction of this molecular circuitry confirmed the surprising role of salt, the researchers said.
“Humans were genetically selected for conditions in sub-Saharan Africa, where there was no salt," Hafler said. “Today, Western diets all have high salt content and that has led to increase in hypertension and perhaps autoimmune disease as well."
He noted all test-tube cell biology is performed based on the salt levels found in blood and not in the tissues where immune cell ultimately travel to fight infections. That may have been a reason salt’s role in autoimmunity has gone undetected.
“We may have been using the wrong concentrations of salt in our experiments for the past half-century," Hafler said. “Nature did not want immune cells to become turned on in the pipeline, so perhaps blood salt levels are inhibitory."
Posts
No comments:
Post a Comment