Abstract 2013

“Neural stem/progenitor cells (NSPCs) have the ability to migrate into the central nervous system (CNS) to replace damaged cells. In inflammatory CNS disease, cytokine transduced neural stem cells may be used as vehicles to specifically reduce inflammation and promote cell replacement. In this study, we used NSPCs overexpressing IL-10, an immunomodulatory cytokine, in an animal model for CNS inflammation and multiple sclerosis (MS). Intravenous injection of IL-10 transduced neural stem/progenitor cells (NSPCIL-10) suppressed myelin oligodendrocyte glycoprotein aa 35--55 (MOG35-55)- induced experimental autoimmune encephalomyelitis (EAE) and, following intravenous injection, NSPC IL-10 migrated to peripheral lymphoid organs and into the CNS. NSPC IL-10 suppressed antigen-specific proliferation and proinflammatory cytokine production of lymph node cells obtained from MOG35-55 peptide immunized mice. In this model, IL-10 producing NSPCs act via a peripheral immunosuppressive effect to attenuate EAE. “  In short IL-10 helps down regulate the inflammation response.

And the disclaimer:  This information is not intended to diagnose, treat, cure or prevent any disease, please consult your healthcare professional.

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             Multiple Sclerosis

  Updated: Dec., 2014  This page is a work in progress

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 From:  Immuno Biology 5 

Multiple Sclerosis is classified as a type IV, T cell-mediated autoimmune disease such as rheumatoid arthritis and insulin-dependent diabetes mellitus.  Following is one approach discussed to mediate the t-cell inflammation response:  “An approach to manipulating the response (inflammation response) is to give cytokines that promote Th1- type responses (to down regulate the inflammation response).  IFN-g, INF-a, IL-10, IL-12 and TGF-b have each been shown to reduce IL-4 stimulated IgE synthesis…”p.490  “…activation (of eosinophils) induces the synthesis of chemical mediators such as prostaglandins, leukotrienes and cytokines…(all involved in the inflammation response)”p.482    “On activation mast cells release chemokines, lipid mediators…cytokines such as IL-4…these mediators contribute to both the acute and chronic inflammatory response.  The lipid mediators, in paricular, act rapidly. …The lipid mediators derive from membrane phospholipids…to release…arachidonic acid.  This molecule can be modified…to give rise to prostaglandins, thromboxanes and leukotrienes….Aspirin…is an inhibitor of the enzyme cyclooxygenase and blocks the production of prostaglandins.”  P.481  Aspirin is derived from White Willow bark (used the make St. John’s cream) and  IL-10’s positive modulating effect  on down regulating the inflammation response is enhanced by the use of Astaxanthin a Vitamin A type, carotenoid.

 From:  Multiple Sclerosis Therapeutics, 2.ed. Cohen & Rudick

“Corticosteroids generally hasten the time to recovery from a clinically significant relapse.  There is no consensus on the optimal formulation, dosage, route of administration, or duration of treatment.”  P.578

Possible supportive protocols:

1.    Astaxanthin:  down-regulate IL-4, up regulate IL-10, crosses the blood/brain barrier.
White willow bark:  NSAD, help control the production of prostaglandins.
Chaparral:  powerful NSAD, help control the production of prostaglandins, up regulates IL-10.
Licorice root:  Help the body increase the production of Cortisal an anti-inflammatory hormone.
Isocort:  an adrenal glandular to help the body increase the production of Cortisal.

6.  Ashwagandha root Tincture.  A tonic containing phytosterols, alkaloids and steroid lactones to mitigate fatigue, to reduce oxidative stress, lessen brain fog, counteract memory loss, increase musclar energy, combat nervous exhaustion and improve sleep quality.  Upon raising the tincture is used to balance the cortisol cycle providing energy and immune regulation.