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» LymeNet Flash » Questions and Discussion » Medical Questions » Molecule linked to autoimmune relapse

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Author Topic: Molecule linked to autoimmune relapse
shazdancer
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We should keep an eye on this, sounds interesting.

http://www.eurekalert.org/pub_releases/2006-12/sumc-mlt120106.php

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david1097
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One thing to remember though is that unlike lupus, MS etc, Lyme has regular flare ups that are closer together and tyically occur on exact cycles. They are also typically not seen in imaging (MRI).

Lupus, MS etc, have flare ups that occur at much less predicatable times, are longer times apart and are easily visible on an MRI.

Right off the bat there are some signficant differences. Still it would seem to me to be an easy thing to check by checking the levels of osteopontin in Lyme patients. (?? brain biopsy or spinal tap required??)

Any volanteers?

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bigmamma
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http://www.nationalmssociety.org/research-2006Dec4.asp

Society-Supported Investigators Uncover Clue to MS Relapses

December 4, 2006

Stanford University researchers have uncovered evidence they believe may explain the role of a protein in the repeated relapses of symptoms experienced by many people with multiple sclerosis, in which the immune system attacks the body's own brain and spinal cord tissues. The study, published early online in the journal Nature Immunology, was funded by the National MS Society, the National Institutes of Health and others.

Drs. Lawrence Steinman, Eun Mi Hur and colleagues identified the culprit protein as osteopontin, which previous studies had shown to be elevated in damaged areas (lesions) of the nervous system of people with MS and to show up in increased levels in the blood plasma prior to the onset of relapses in people with MS. Osteopontin has many different jobs in the body, such as the maintenance of bones, and has also been linked to other immune diseases including rheumatoid arthritis and lupus erythematosus.

The investigators worked with various mouse models of MS, and in mice that had normal levels of osteopontin versus those that were engineered to lack the protein. In a series of experiments, the team found that osteopontin could stimulate repeated relapses and enhance disease progression, and inhibit spontaneous recovery from symptoms. This resulted in much more severe disease than in those with normal levels of the protein.

When the immune system is doing its normal job, such as fighting off a viral infection, the immune cells that are activated to launch the attack eventually die off when the infection has been neutralized. In researching how osteopontin inhibited normal recovery from symptoms, Dr. Steinman's team found that the protein enhanced the survival of activated immune cells. The team also identified several specific mechanisms through which this protein inhibited their usual elimination from the system.

This research may lead to new therapeutic approaches that target osteopontin. However, because this protein has multiple functions in the body, additional research should help pinpoint ways to inhibit its influence on the immune attack without altering its ability to do other jobs in the body.

-- Research and Clinical Programs

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bigmamma
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David,

I have lesions on my brain from Lyme, as many others do. Some say that lyme flairs every 28 days and some believe it should have an exact cycle, but patient evidence does not always agree with that. Many here have more or less frequent lyme symptom flairs.

Symptoms of Lyme and MS are very, very similar for many.

Visit this website and read the patient stories and I guarrantee people will be saying - Do they have Lyme or Do I have MS?
www.faceofms.org

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bigmamma
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Shaz,

Here is some interesting genetic autoimmune research as well. Visit http://www.madgc.org

What is the Multiple Autoimmune Disease Genetics Consortium (MADGC)?

MADGC is a group of leading genetic researchers who have joined efforts to identify and understand the genes that autoimmune diseases have in common. This research may ultimately give doctors valuable knowledge about the basic causes of autoimmune disease and allow them to better diagnose and treat patients.

Who is eligible to participate?

If at least two members of your family have different autoimmune diseases from the list displayed on the right, your family may be eligible to participate.

Rheumatoid Arthritis
Juvenile Rheumatoid Arthritis
Systemic Lupus
Multiple Sclerosis
Autoimmune Thyroid Disease (Graves' or Hashimoto's)
Type I Diabetes (Insulin Dependent)
Psoriasis
Inflammatory Bowel Disease (Crohn's Disease or Ulcerative Colitis)
Primary Sjgrens

What are autoimmune diseases?

Autoimmune diseases encompass a broad range of diseases in which a person's immune system attacks his or her own healthy tissue. They are not directly inherited from one generation to the next. A combination of genes, environmental factors (such as exposure to cigarette smoke or certain viruses), chance and time determine who is most likely, or susceptible, to develop an autoimmune disease.

(Supported by The National Institute of Allergy and Infectious Diseases

We anticipate that recruitment activities will resume early in 2007. You are welcome to submit a message to us. Thank you for your interest.

North Shore - Long Island Jewish Health System - New York

The Feinstein Institute for Medical Research

Toll Free : 1-877-698-9467

E-mail :
Marlena Kern, RN [email protected]

****Hmmm, I wonder if these samples were checked for Lyme disease?

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Sojourner
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quote:
Originally posted by david1097:
One thing to remember though is that unlike lupus, MS etc, Lyme has regular flare ups that are closer together and tyically occur on exact cycles. They are also typically not seen in imaging (MRI).

Lupus, MS etc, have flare ups that occur at much less predicatable times, are longer times apart and are easily visible on an MRI.

Right off the bat there are some signficant differences. Still it would seem to me to be an easy thing to check by checking the levels of osteopontin in Lyme patients. (?? brain biopsy or spinal tap required??)

Any volanteers?

Where exactly did you get your info about the nature of the differences between MS and Lyme? I don't think your conclusions are correct. In fact, Lyme and MS can present exactly the same--same symptoms, same diagnostics (MRIs)

Couple of interesting notes on Osteopontin:

OPN (Osteopontin)has been shown to control the growth of intracellular bacteria.

Here's some research regarding OPN and Lyme:

In vitro, OPN has both pro- and anti-inflammatory properties. Nitric oxide production by macrophages is suppressed in the presence of OPN, suggesting an anti-inflammatory role (19, 45). Recently, Ashkar and colleagues demonstrated a proinflammatory action of OPN (4). OPN independently stimulates the production of interleukin-12 (IL-12) by macrophages while downregulating the production of IL-10 by macrophages stimulated with lipopolysaccharide (LPS). Both IL-10 and IL-12 have been implicated in the regulation of murine Lyme arthritis (2, 3, 10).

Many of the properties of Opn suggest it as a candidate gene for regulation of the host response to B. burgdorferi infection and development of Lyme arthritis: (i) the involvement of OPN in inflammation and regulation of IL-12 and IL-10, bone remodeling, wound repair, and the immune response to pathogens; (ii) the physical position of OPN within a linkage group on chromosome 5; and (iii) the fact that severely and mildly arthritic strains of mice possess distinct alleles for OPN implicated in resistance to other bacteria. The development of mice with a targeted disruption in the OPN gene allowed assessment of its involvement in host response to B. burgdorferi.

Here's the link: In vitro, OPN has both pro- and anti-inflammatory properties. Nitric oxide production by macrophages is suppressed in the presence of OPN, suggesting an anti-inflammatory role (19, 45). Recently, Ashkar and colleagues demonstrated a proinflammatory action of OPN (4). OPN independently stimulates the production of interleukin-12 (IL-12) by macrophages while downregulating the production of IL-10 by macrophages stimulated with lipopolysaccharide (LPS). Both IL-10 and IL-12 have been implicated in the regulation of murine Lyme arthritis (2, 3, 10).

Here's the link:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127811&tools=bot

I think it's important that we don't get locked into the same compartmentalized thinking that the research establishment does----there are major connections between these diseases that are often overlooked

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bigmamma
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Could this be the cause of my very high serum calcium levels when at my sickest?

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david1097
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If I am not mistaken, MS replases and recoveries take several weeks to appear then disappear on MRI images. Lyme cycles tytpically occur on 4 week intervals between peaks, some even faster.

Also, I have read fallons work and there is no mention or indication of recovery frmn MRI lessions with Lyme until antibtiotics are used.

While the lessions on a single MRI may look the same between Lyme and MRI, the more typical, relapsing and remitting type discussed in the paper that was quoted, will resutl in demyelation that is detectable by MRI, appearing and disappearing. This is one of the reason why multple time seperated MRI's are needed for a definative MS diagnosis.

If it a case of non remitting, progressive then Lyme and MS are hard to tell appart via MRI but the paper in this case specifically refered to relapsing/remitting.

I hope that clarifies my post.

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