Health Boards
We all know the benefits of sea water for psoriasis, especially the Dead Sea salt and there is lots of information. But what about salt intake via our diet, could salt be bad for psoriasis?
![[Image: Saltmill.jpg]](https://upload.wikimedia.org/wikipedia/commons/d/d8/Saltmill.jpg)
Three studies published today in Nature suggest that salt may cause to many T-Cells, and we all know to many T-Cells is not good. You didn't know that? See Here: T Cells the soldiers in your body
OK back to these three studies.
All this evidence, Kuchroo says, “is building a very interesting hypothesis that salt may be one of the environmental triggers of autoimmunity”.
But Kuchroo and other researchers say that evidence so far cannot predict the effect of salt on human autoimmunity. “As a physician, I’m very cautious,” Hafler says. “Should patients go on a low-salt diet? Yes,” he says, adding that “people should probably already be on a low-salt diet” for general health concerns.
Other experts are intrigued by the findings. “They have a very clear effect in vitro,” says John O’Shea, scientific director of the National Institute of Arthritis and Musculoskeletal and Skin Diseases Intramural Research Program in Bethesda, Maryland. But Hafler and others note that there are likely many cell types and environmental factors involved in triggering autoimmunity.
The results offer tantalizing leads for drug targets for autoimmune conditions. But O’Shea notes that it is unclear whether TH17 proliferation is a factor in all autoimmune disease. A targeted drug that might work to relieve psoriasis might not subdue rheumatoid arthritis. “When we say autoimmunity, we’re implying that it’s one thing,” O’Shea says. “But it’s not one thing — it’s heterogeneous.”
Source: nature.com
So there you have it. Although Sea Salt is good for your skin by applying it directly, it's not so good for you if taken internally.
But Wait! Don't we absorb things through our skin?
*There's a bit of conflicting advice on the recommended salt intake. But the NHS U.K recommend that Adults should eat no more than 6g of salt a day – that's around one full teaspoon. And that is not just the salt you put on your food, it takes into account the salt already in foods either naturally or processed. (If you ate just half a tin of baked beans on two slices of toast, you'd be reaching your daily salt limit.)
Three studies published today in Nature suggest that salt may cause to many T-Cells, and we all know to many T-Cells is not good. You didn't know that? See Here: T Cells the soldiers in your body
OK back to these three studies.
Quote:
#1 Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1.
TH17 cells (interleukin-17 (IL-17)-producing helper T cells) are highly proinflammatory cells that are critical for clearing extracellular pathogens and for inducing multiple autoimmune diseases. IL-23 has a critical role in stabilizing and reinforcing the TH17 phenotype by increasing expression of IL-23 receptor (IL-23R) and endowing TH17 cells with pathogenic effector functions. However, the precise molecular mechanism by which IL-23 sustains the TH17 response and induces pathogenic effector functions has not been elucidated. Here we used transcriptional profiling of developing TH17 cells to construct a model of their signalling network and nominate major nodes that regulate TH17 development. We identified serum glucocorticoid kinase 1 (SGK1), a serine/threonine kinase, as an essential node downstream of IL-23 signalling. SGK1 is critical for regulating IL-23R expression and stabilizing the TH17 cell phenotype by deactivation of mouse Foxo1, a direct repressor of IL-23R expression. SGK1 has been shown to govern Na+ transport and salt (NaCl) homeostasis in other cells. We show here that a modest increase in salt concentration induces SGK1 expression, promotes IL-23R expression and enhances TH17 cell differentiation in vitro and in vivo, accelerating the development of autoimmunity. Loss of SGK1 abrogated Na+-mediated TH17 differentiation in an IL-23-dependent manner. These data demonstrate that SGK1 has a critical role in the induction of pathogenic TH17 cells and provide a molecular insight into a mechanism by which an environmental factor such as a high salt diet triggers TH17 development and promotes tissue inflammation.
#2Dynamic regulatory network controlling TH17 cell differentiation.
Despite their importance, the molecular circuits that control the differentiation of naive T cells remain largely unknown. Recent studies that reconstructed regulatory networks in mammalian cells have focused on short-term responses and relied on perturbation-based approaches that cannot be readily applied to primary T cells. Here we combine transcriptional profiling at high temporal resolution, novel computational algorithms, and innovative nanowire-based perturbation tools to systematically derive and experimentally validate a model of the dynamic regulatory network that controls the differentiation of mouse TH17 cells, a proinflammatory T-cell subset that has been implicated in the pathogenesis of multiple autoimmune diseases. The TH17 transcriptional network consists of two self-reinforcing, but mutually antagonistic, modules, with 12 novel regulators, the coupled action of which may be essential for maintaining the balance between TH17 and other CD4+ T-cell subsets. Our study identifies and validates 39 regulatory factors, embeds them within a comprehensive temporal network and reveals its organizational principles; it also highlights novel drug targets for controlling TH17 cell differentiation.
#3Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells.
There has been a marked increase in the incidence of autoimmune diseases in the past half-century. Although the underlying genetic basis of this class of diseases has recently been elucidated, implicating predominantly immune-response genes, changes in environmental factors must ultimately be driving this increase. The newly identified population of interleukin (IL)-17-producing CD4+ helper T cells (TH17 cells) has a pivotal role in autoimmune diseases. Pathogenic IL-23-dependent TH17 cells have been shown to be critical for the development of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, and genetic risk factors associated with multiple sclerosis are related to the IL-23–TH17 pathway. However, little is known about the environmental factors that directly influence TH17 cells. Here we show that increased salt (sodium chloride, NaCl) concentrations found locally under physiological conditions in vivo markedly boost the induction of murine and human TH17 cells. High-salt conditions activate the p38/MAPK pathway involving nuclear factor of activated T cells 5 (NFAT5; also called TONEBP) and serum/glucocorticoid-regulated kinase 1 (SGK1) during cytokine-induced TH17 polarization. Gene silencing or chemical inhibition of p38/MAPK, NFAT5 or SGK1 abrogates the high-salt-induced TH17 cell development. The TH17 cells generated under high-salt conditions display a highly pathogenic and stable phenotype characterized by the upregulation of the pro-inflammatory cytokines GM-CSF, TNF-α and IL-2. Moreover, mice fed with a high-salt diet develop a more severe form of EAE, in line with augmented central nervous system infiltrating and peripherally induced antigen-specific TH17 cells. Thus, increased dietary salt intake might represent an environmental risk factor for the development of autoimmune diseases through the induction of pathogenic TH17 cells.
All this evidence, Kuchroo says, “is building a very interesting hypothesis that salt may be one of the environmental triggers of autoimmunity”.
But Kuchroo and other researchers say that evidence so far cannot predict the effect of salt on human autoimmunity. “As a physician, I’m very cautious,” Hafler says. “Should patients go on a low-salt diet? Yes,” he says, adding that “people should probably already be on a low-salt diet” for general health concerns.
Other experts are intrigued by the findings. “They have a very clear effect in vitro,” says John O’Shea, scientific director of the National Institute of Arthritis and Musculoskeletal and Skin Diseases Intramural Research Program in Bethesda, Maryland. But Hafler and others note that there are likely many cell types and environmental factors involved in triggering autoimmunity.
The results offer tantalizing leads for drug targets for autoimmune conditions. But O’Shea notes that it is unclear whether TH17 proliferation is a factor in all autoimmune disease. A targeted drug that might work to relieve psoriasis might not subdue rheumatoid arthritis. “When we say autoimmunity, we’re implying that it’s one thing,” O’Shea says. “But it’s not one thing — it’s heterogeneous.”
Source: nature.com
So there you have it. Although Sea Salt is good for your skin by applying it directly, it's not so good for you if taken internally.
But Wait! Don't we absorb things through our skin?
*There's a bit of conflicting advice on the recommended salt intake. But the NHS U.K recommend that Adults should eat no more than 6g of salt a day – that's around one full teaspoon. And that is not just the salt you put on your food, it takes into account the salt already in foods either naturally or processed. (If you ate just half a tin of baked beans on two slices of toast, you'd be reaching your daily salt limit.)
