alphaB-crystallin protein

[gwa]

anecdote,

I would like to get your husband's opinion about the discovery of the alphaB-crystallin protein made by researchers at Stanford and whether it could be related to CPN bacteria.

This report was posted earlier here on general forums , but I am including some parts of the post now.

"http://med.stanford.edu/news_releases/2 ... inman.html

A protein found primarily in the lens of the eye could be the critical “tipping point” in the spiral of inflammation
and damage that occurs in multiple sclerosis, researchers at the Stanford University School of Medicine report.

This protein—alphaB-crystallin—is not normally found in the brain, but develops in response to the injuries
inflicted on nerve cells by multiple sclerosis. The nerve-cell injuries can cause people to suffer loss of motor
control and even paralysis.

The recognition of this protein’s role in multiple sclerosis began more than a decade ago, when Dutch researcher
Johannes van Noort, PhD, found that the main stimulant of the immune system’s attack on the brain was not the
presumed culprit of one of the parts of myelin, but alphaB-crystallin, the major structural protein of the lens
of the eye.

gwa

[SarahLonglands]

gwa, I've sent this plus the whole link to David, but will in the meantime make a little answer myself, to see how close we both come to the
same conclusion. Some pathogens, including chlamydia pneumoniae and EBV (to be fair to Ian) have the ability to move certain things about the body so they can be found in unexpected places, hence alpha B-crystallin protein could well be found in the brain of someone with MS, so get rid of the pathogen, no more damage caused by MS, no more migration of the protein.

Sarah

[SarahLonglands]

Now I've got a reply from David:

gwa, I don’t know much about alpha B crystallin except that it’s a major protein in the lens of the eye and has been proposed as an auto-antigen in MS. Many proteins have been posited as auto-antigens in MS, including Myelin Oligodendrocyte Glycoprotein and a number of Heat Shock Proteins and others. In fact alpha B crystellin is itself a member of the small-HSP family. The fact that there are such a plethora of potential ‘auto-antigens’ casts doubt on the whole auto-immune theory. Occam’s razor suggests that they are all likely to be secondary; indeed, a covert chronic infection with an intracellular pathogen would disarrange a number of host systems. And in fact this has been shown; antibodies to C. pneumoniae specific HSP60 have been found in the CSF of persons with MS. Bacterial HSP60 is upregulated in persistent infection and is highly antigenic; the antibodies so produced may act against mammalian analogues. This has been termed molecular mimicry. HSPs are good candidates for this because they are highly conserved. Interestingly, most bacteria possess genes for alpha crystallins, though apparently not chlamydiae..

One other factor is that chronic infections with C. pneumoniae breach the blood-brain barrier; in addition macrophage / microglia cell types are very actively motile and it’s conceivable that they transfer proteins to places where they are not normally found. C. pneumoniae causes eye infections, including uveitis, retinal vasculitis and macular degeneration, and associated inflammation may break down the barrier between eye and CNS.

As far as I can see, the presence of alpha B crystallin is found in the CSF in a number of neurological conditions and is not specifically found in MS. I know very little about this, but to speculate on its being an autoantigen would mean that you would have to buy into an autoimmune theory; evidence supporting primary autoimmunity is looking increasingly shaky. The fact that carriers of a certain rare genotype of alpha B crystallin have a particular variant of MS (with a non-inflammatory, rapidly neurodegenerative course) doesn’t detract from the idea of a primary chronic infection. Many chronic infections (such as TB and leprosy) take on a particular clinical appearance depending upon the host’s genetic inheritance.

[gwa]

anecdote,

Please thank your husband for his reply. I have read it several times and am beginning to digest what he is explaining.

When I first read about Dr Steinman's discovery, I was reminded about my own first symptom which was optic neuritis. Thus, I wondered if the protein was the instigator of the disease.

This part of Dr Wheldon's explanation is what I was questioning about the protein and its relationship to MS:

"The fact that carriers of a certain rare genotype of alpha B crystallin have a particular variant of MS (with a non-inflammatory, rapidly neurodegenerative course) doesn’t detract from the idea of a primary chronic infection. Many chronic infections (such as TB and leprosy) take on a particular clinical appearance depending upon the host’s genetic inheritance."


gwa

[SarahLonglands]

gwa, you might care to look at this thread:

http://www.thisisms.com/ftopicp-17703-o ... itis#17703 from August last year.

I have a copy of the whole paper if you would like it.

Sarah

[gwa]

anecdote,

Please send me the copy of the paper on ON. I would like to read the whole thing.

gwa

[SarahLonglands]

Will do!