Children who eat too much dietary salt could be setting themselves up for developing autoimmune diseases, a new study reports. Increased dietary salt intake can induce a group of aggressive immune cells that are involved in triggering and sustaining autoimmune diseases.
The immune system attacks healthy tissue instead of fighting pathogens in autoimmune diseases. Autoimmune diseases arise from an inappropriate immune response of the body against substances and tissues normally present in the body. It's an overactive immune response of the body against substances and tissues normally present in the body. The body actually attacks its own cells. And excess salt may play an important role in autoimmune diseases, says a new study published online in the March 6, 2013 issue of the journal Nature.
Too much salt in foods fed to children and adults is an issue that has been brought by consumers and health professionals to food manufacturers and eateries for at least a decade. In fact, on August 21, 2012 restaurant chain, Boston Market announced that it planned to remove salt shakers from tables at all of its locations and will launch plans to reduce sodium levels by 20 percent in three popular foods -rotisserie chicken, macaroni and cheese and mashed potatoes.
How much excess salt kids are putting on their food adds upon the excess salt already in processed foods such as canned, frozen, and packaged foods bought at supermarkets. The big issue is how excess salt in the diet plays a role in the development of autoimmune diseases, even if a person isn't salt-sensitive or whether or not there's a family history of kidney disease or high blood pressure.
Excess salt's role in autoimmune diseases
How too much dietary salt may play an important role in autoimmune diseases is explained in two new papers published March 6, 2013 in the journal Nature. Exposure to high levels of salt has been found to make both cultured mouse and human T cells more pathogenic. High-salt diets worsened autoimmune disease in mice, the new study reports.
The first research team, based at Harvard University, the Massachusetts Institute of Technology (MIT), and the Broad Institute, came to investigate salt in a roundabout way. Some forms of T helper cells, called T helper 17 (TH17) cells, have been implicated in a variety of autoimmune diseases, and the researchers wanted to understand what makes naive, immature T cells differentiate into pathogenic ones. Examples of autoimmune diseases are multiple sclerosis, lupus, and psoriasis, and there are many more caused when the body's immune system attacks the body as if it were an invading virus or bacteria or a foreign object in the body that needs to be rejected.
In recent decades scientists have observed a steady rise in the incidence of autoimmune diseases in the Western world. Since this increase cannot be explained solely by genetic factors, researchers hypothesize that the sharp increase in these diseases is linked to environmental factors.
Among the suspected culprits are changes in lifestyle and dietary habits in developed countries, where highly processed food and fast food are often on the daily menu. These foods tend to have substantially higher salt content than home-cooked meals.
This new study is the first to indicate that excess salt intake may be one of the environmental factors driving the increased incidence of autoimmune diseases. You can read the original study's abstract, "Sodium Chloride Drives the Induction of Pathogenic Th17 Cells." Check out the abstract.
You can read the original study or its abstract from one of the researchers and team, C. Wu et al., “Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1,” Nature, 2013. Or check out the study from another researcher and team, M. Kleinewietfeld, “Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells,” Nature March 6, 2013. You also can read about the study from another researcher and team, N. Yosef, “Dynamic regulatory network controlling TH17 cell differentiation,” Nature.
High salt conditions boost the induction of pathogenic Th17 cells in humans
This process is highly specific and dependent on the ancient stress related pathway of p38/MAPK, NFAT5 and SGK1. Thus, increased dietary salt intake might represent an environmental risk factor for the development of autoimmune diseases like MS through the induction of pathogenic Th17 cells, the study concluded, according to its abstract. See the article, Salt at Fault? | The Scientist Magazine®
A few years ago Jens Titze showed that excess dietary salt (sodium chloride) accumulates in tissue and can affect macrophages (a type of scavenger cells) of the immune system. Independent of this study, Markus Kleinewietfeld and David Hafler observed changes in CD4 positive T helper cells (Th) in humans, which were associated with specific dietary habits.
The question arose whether salt might drive these changes and thus can also have an impact on other immune cells. Helper T cells are alerted of imminent danger by the cytokines of other cells of the immune system. They activate and "help" other effector cells to fight dangerous pathogens and to clear infections.
A specific subset of T helper cells produces the cytokine interleukin 17 and is therefore called Th17 for short. Evidence is mounting that Th17 cells, apart from fighting infections, play a pivotal role in the pathogenesis of autoimmune diseases. Multiple sclerosis is one example of an autoimmune disease.
Salt dramatically boosts the induction of aggressive Th17 immune cells
In cell culture experiments the researchers showed that increased sodium chloride can lead to a dramatic induction of Th17 cells in a specific cytokine milieu. "In the presence of elevated salt concentrations this increase can be ten times higher than under usual conditions," Markus Kleinewietfeld and Dominik Müller explained in the March 6, 2013 news release, "International study: Excess dietary salt may drive the development of autoimmune diseases." Under the new high salt conditions, the cells undergo further changes in their cytokine profile, resulting in particularly aggressive Th17 cells.
In mice, increased dietary salt intake resulted in a more severe form of experimental autoimmune encephalomyelitis, a model for multiple sclerosis. Multiple sclerosis is an autoimmune disease of the central nervous system in which the body's own immune system destroys the insulating myelin sheath around the axons of neurons and thus prevents the transduction of signals, which can lead to a variety of neurological deficits and permanent disability. Recently, researchers postulated that autoreactive Th17 cells play a pivotal role in the pathogenesis of multiple sclerosis.
Those Th17 cells in the nervous system of the mice increased under a high salt diet, an important contribution to the understanding of multiple sclerosis
Interestingly, according to the researchers, the number of pro-inflammatory Th17 cells in the nervous system of the mice increased dramatically under a high salt diet. The researchers showed that the high salt diet accelerated the development of helper T cells into pathogenic Th17 cells. The researchers also conducted a closer examination of these effects in cell culture experiments and showed that the increased induction of aggressive Th17 cells is regulated by salt on the molecular level.
"These findings are an important contribution to the understanding of multiple sclerosis and may offer new targets for a better treatment of the disease, for which at present there is no known cure," said Ralf Linker, according to the news release, "International study: Excess dietary salt may drive the development of autoimmune diseases." Dr. Linker, as head of the Neuroimmunology Section and Attending Physician at the Department of Neurology, University Hospital Erlangen, seeks to utilize new laboratory findings for the benefit of patients.
Psoriasis is another autoimmune disease with strong Th17 components
Besides multiple sclerosis, Dominik Müller and his colleagues want to study psoriasis, another autoimmune disease with strong Th17 components. The skin, as Jens Titze recently discovered, also plays a key role in salt storage and affects the immune system.
"It would be interesting to find out if patients with psoriasis can alleviate their symptoms by reducing their salt intake," the researchers said. "However, the development of autoimmune diseases is a very complex process which depends on many genetic and environmental factors," the immunologist Markus Kleinewietfeld said in the news release.
"Therefore, only further studies under less extreme conditions can show the extent to which increased salt intake actually contributes to the development of autoimmune diseases." Also see the site, Helmholtz Association of German Research Centers. The study is, "Sodium Chloride Drives the Induction of Pathogenic Th17 Cells." Authors include: Markus Kleinewietfeld1, 2*, Arndt Manzel3, 4, Jens Titze5, 6, Heda Kvakan7, 8, Nir Yosef2, Ralf A. Linker3, Dominik N. Muller7,9+, David A. Hafler1, 2*+.
The study also was conducted by the research team which includes the following: Dr. Markus Kleinewietfeld, Prof. David Hafler (both Yale University, New Haven and the Broad Institute of the Massachusetts Institute of Technology, MIT, and Harvard University, USA), PD Dr. Ralf Linker (Dept. of Neurology, University Hospital Erlangen), Professor Jens Titze (Vanderbilt University and Friedrich-Alexander-Universität Erlangen-Nürnberg, FAU, University of Erlangen-Nuremberg) and Professor Dominik N. Müller (Experimental and Clinical Research Center, ECRC, a joint cooperation between the Max-Delbrück Center for Molecular Medicine, MDC, Berlin, and the Charité – Universitätsmedizin Berlin and FAU) (Nature).