Chronic Inflammation in the Body | Treatment

Multiple sclerosis (MS) is generally regarded as an autoimmune disease – one in which the immune system mistakenly attacks a part of the body – in this case the covering of neurons in the central nervous system.

Without their insulating cover, the nerves do not function properly. MS can result in widely varying symptoms depending on which nerves are ‘attacked.’

The study abstract summarized below does not directly reference multiple sclerosis. But it does suggest one possible mechanism by which an initially small lesion could progress, and how the disease might be self-sustaining.

Damage to the nerve covering – the myelin sheath – releases sulfatide. Sulfatide then triggers inflammation via activation of NF-kB. The inflammation leads to further damage to the nerve sheath, further release of sulfatide, more NF-kB activation, more inflammation, etc.

It seems likely that those without multiple sclerosis suffer occasional damage to a myelin sheath, but that such damage does not become progressively worse, despite the release of sulfatide.

It may be that the immune system of those who do not suffer with multiple sclerosis is better able to shut down inflammation and prevent the vicious cycle from developing.

Perhaps by providing supplemental NF-kB inhibitors we could prevent self-perpetuating inflammation in multiple sclerosis, or at least reduce the severity of that inflammation – thereby lessening damage and speeding the onset of remission.

Dendritic cells stimulate the immune system by presenting antigens (foreign particles) to other immune cells and by causing the release of pro-inflammatory cytokines. It is believed that dendritic cells may play an important role in autoimmune disease.

The serum from patients with lupus causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.

The serum from patients with asthma also causes monocytes to transform into dendritic cells and is associated with increased NF-kB activation.

Inhibition of NF-kB contributes to T cell tolerance – by which is meant tolerance to self. When “tolerant” T cells do not attack self. T cell intolerance may lead to autoimmune disease.

Studies have suggested involvement of interleukin 17 (IL-17) in autoimmune diseases, although its effect on B cell biology has not been clearly established.

Here we demonstrate that IL-17 alone or in combination with B cell-activating factor controlled the survival and proliferation of human B cells and their differentiation into immunoglobulin-secreting cells. This effect was mediated mainly through the nuclear factor-kappaB-regulated transcription factor Twist-1.

Multiple sclerosis (MS) is a chronic inflammatory, demyelinating and neurodegenerative disorder of the central nervous system (CNS) of unknown cause.

We do not know its cause, and we have yet to identify an ideal treatment, but what we do know is:

* NF-kB is a central player in the activation of T cells, B cells, dendritic cells, macrophages, and CNS resident glia – all of which are believed to be important in MS disease progression.

* NF-kB is induced by a large number of extracellular signals and its activation results in both increased production of pro-inflammatory cytokines and increased production of antibody by B cells.

* IL-17 is probably a key player in MS as well as other autoimmune conditions, and it is a potent activator of NF-kB.

* Activation of NF-kB in microglial cells and astrocytes of MS patients is known to result in the production of proinflammatory cytokines and potentially neurotoxic mediators.

* Some drugs currently used in the treatment of MS, such as beta-interferon, are thought to act primarily via inhibition of NF-kB.

* Curcumin, a major constituent of turmeric, has recently been shown to be effective in the treatment of a wide variety of diseases, including cancer, infection, and autoimmune disease. Curcumin inhibits production of IL-17, and appears to act by inhibiting NF-kB.

* Many MS patients have a reduced frequency of relapses during pregnancy, due at least in part to altered levels of estrogens. Studies suggest that estrogens inhibit NF-kB, leading to reduced T cell transmigration into the CNS in MS patients and reduced cytokine production.

Taken together, these findings suggest the potential therapeutic benefit of NF-kB inhibition.

An NF-kB inhibitor would make a great treatment for pain and inflammation. That is true. What’s surprising, or not, is that neither in the abstract nor in the full article are any of the useful NF-kB inhibitors found in nature mentioned. You would think the author would at least give a hat tip to some of the more common and more popular natural products that are known to inhibit NF-kB.

Even the federal government (USDA) recommends increasing your intake of fruits and vegetables, in part because a higher dietary intake, especially of dark green, deep yellow and other colorful fruits, will reduce your risk of cancer.

BENLYSTA inhibits the biological activity of B-lymphocyte stimulator, or BLyS. BLyS is a naturally occurring protein which is required for the survival and development of B-lymphocyte cells into mature plasma B cells.

Plasma B cells produce antibodies, the body’s first line of defense against infection. In lupus and certain other autoimmune diseases, elevated levels of BLyS are believed to contribute to the production of autoantibodies – antibodies that attack and destroy the body’s own healthy tissues. The results of prospective observational studies show a significant correlation of elevated levels of BLyS with SLE disease activity.