Why Braggs Vinegar may be helping pain

[Guest guest]

Joanne, since I heard about the vinegar I wondered if it was affecting the white

blood cells and that they were causing pain... well take a look at this article.

T cells causing inflammation in autoimmune disease are white blood cells.

Well since ancient Indian times (India), it is known that vinegar kills white

blood cells. I think there is a connection with the Braggs reducing pain and

killing white blood cells. Read below about blocking IL-17 and pain reduction,

which IL-17 is a T cell:

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New immune cell found to be a key to inflammatory diseases

nächste Meldung 04.10.2005

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The molecular roots of inflammatory and autoimmune diseases such as asthma,

arthritis, and multiple sclerosis (MS) have been discovered by a team of

researchers led by The University of Texas M. D. Cancer Center. They

say their findings may point to ways to effectively treat these diseases - if

not stop them before they start.

In a lead article in the November issue of Nature Immunology (released online on

Oct. 2), the scientists report finding a novel type of " T helper " cell they say

is the culprit for initiating chronic inflammation and autoimmunity in a variety

of body tissues. This newly described T cell - which they call inflammatory TH

cells (or THi) - produces interleukin 17 (IL-17), a potent cytokine that

researchers have already linked to an immune system gone awry.

" We suspected that IL-17 is a player in autoimmune and inflammatory diseases,

but we didn't understand where IL-17 came from before this finding, " says the

study's lead investigator, Chen Dong, Ph.D., an associate professor in the

Department of Immunology.

" Now we have discovered the source of IL-17 and also have solidly demonstrated

that these are the crucial cells that regulate tissue inflammation in autoimmune

disease and asthma, " he says. " These findings suggest that shutting down the

activity of these THi cells might stop chronic inflammatory diseases from

developing in the first place. "

He adds that while such drugs are years away from development and clinical

trials, agents that block IL-17 could represent an effective treatment, based on

these results.

Dong and four other M. D. researchers collaborated with scientists from

the University of Washington, the Institute for Systems Biology in Seattle and

s Hopkins School of Medicine.

While the findings have no immediate relevance to the field of oncology, it is

known that cancer can arise from inflammatory processes. Further understanding

of how the immune system functions, and how it can go awry, is important, Dong

says.

T cells are white blood cells that play a variety of roles in the immune system,

including the identification of foreign molecules in the body, such as bacteria

and viruses, and the activation and deactivation of other immune cells.

T helper cells are specific T cells that have receptors that recognize and bind

to fragments (known as antigens) of the invaders that already have been

displayed on the surface of other immune system cells. (These T helper cells are

also called CD4 T cells since they express CD4 molecules.) Once the antigen has

been bound, these T helper cells become activated, and they morph into

" effector " cells which then boost an immune response by secreting " cytokine "

molecules such as interleukins and interferons.

Before this study, two such different types of effector T helper cells had been

known - type I (TH1), linked to the body's response to microbial infection, and

type 2 (TH2), which plays a crucial function in production of B cell antibodies

and also is associated with development of allergies.

Although TH1 and TH2 are known to produce powerful cytokines - such as

interferon-gamma (IFN-g) and allergy-associated interleukin 4 (IL-4),

respectively - they are not inflammatory or associated with production of IL-17,

which sets off an errant immune response that results in tissue inflammation.

Researchers could not understand the origins of such an inflammatory response in

body tissues. The only clue they had was that excess IL-17 molecules are found

in arthritic joints, in lungs swollen by asthma and in brain cells that lead to

nerve degeneration and the onset of MS. " But we didn't know which T cells were

responsible for secreting IL-17, " Dong says. To find out where IL-17 came from,

the researchers designed a series of cell culture studies and mouse experiments.

In brief, they " educated " T helper cells to become IL-17 producing cells. They

found that IL-17 is triggered by a unique set of signals that now define this

new " lineage " of T helper cells. " They are completely different from TH1 and TH2

effector cells, " says Dong. They then used a mouse model of MS and demonstrated

that they could stop development of the disease with an antibody agent that

blocked IL-17. Finally, they developed a transgenic mouse model of asthma and

found that, by producing excessive IL-17 in the lung, they were able to produce

asthmalike symptoms.

Dong says the researchers hypothesize that these newly discovered THi cells

travel to selected body tissues and release IL-17. This action, in turn,

stimulates expression of " chemokines, " which results in a rush of inflammatory

cells into the tissue. Thus a chronic inflammatory reaction is set up, he says.

The scientists don't know what initially sets off activation of the newly

discovered T helper cell in diseases such as arthritis and asthma, Dong says.

" We don't know why these dangerous helper T cells are activated in the patients,

but we now know how they function, and that should take us a long way to

understanding and treating these and other inflammatory and autoimmune

diseases. "