JOURNAL OF INDEPENDENT MEDICAL RESEARCH
"Putative Antibacterial Mechanisms for Angiotensin II Receptor Blockers"
Authors: Trevor G Marshall, PhD1, Belinda Fenter, BS2, and Frances E Marshall, GradDipPharm, RPh3
http://www.joimr.org/phorum/read.php?f=2&i=53&t=53
That's HOT off the press!...Published (electronically) just a few hours ago, TODAY no less.
I had heard that this article was supposed to come out soon, but it hasn't even been posted at the SarcInfo website YET (as of a few minutes ago, when I checked there for notice of it.)
Nice job, Barb!
"Generally regarded as such; supposed."
Theroretical, not proven. Big difference.
Here's something that HAS been proven:
Characterization of the physiological requirements for the bactericidal effects of a monoclonal antibody to OspB of Borrelia burgdorferi by confocal microscopy.
The bactericidal effect of Fab-CB2 is not dependent on the induction of spirochetal proteases but is dependent on the presence of Ca2+ and Mg2+.
Supplementation of Ca2(+)- and Mg2(+)-free medium with these cations restored the bactericidal effects of Fab-CB2.
The mechanism by which a Fab fragment of an antibody destroys a bacterium directly may represent a novel form of antibody-organism interaction.
PMID: 9125579
[This message has been edited by Marnie (edited 12 May 2004).]
Regarding Marshall's paper, I've attempted to read it but it is so far over my head that I'm having great difficulty understanding it.
Remember, we lay persons are at a great disadvantage here because the articles in this journal are not peer-reviewed prior to publication, as are the articles in other medical journals.
That's why I'm waiting to see what critical comments others, who have the scientific background to understand it, will say on the JOIMR website about this paper.
Having said that, however, we should all be aware that the current method of peer-review by most other major medical journals is seriously flawed. That's why this new method of rapid communication via electronic journals is the wave of the future.
We, as lay persons, however, must take careful notice of what critical comments are posted, following publication of such articles. Likewise, we must be careful to discern the qualifications of those persons who make critical comments, whether favorable critiques or unfavorable criticisms.
This is something very subtle, which persons who are not used to reading lots of medical journal articles, might overlook. Thus, it needs to be mentioned -- so that we can all keep this fact in mind whenever we read any of Marshall's work.
That seems to be the theory anyway.
In a dish, or in a human.
We know the following:
E. Required by immunological process. Magnesium, immunity, and allergy: Mg is required for several steps of immunological reactions
1. Lymphoblastic transformation, a prerequisite of secretion of antibodies by lymphoblasts, requires Ca2+ and Mg2+
2. Mg is required for synthesis of proteins, immunoglobulins included (immunoglobulins are antibodies)
3. Antibody-induced complement activation is Mg dependent
4. The antigen-immunoglobulin-complement reaction induces degranulation of the mastocyte
http://www.mdschoice.com/elements/elements/major_minerals/magnesium.htm
"The levels of antibodies (immunoglobulins) decrease in experimental animals (mice, rats and hamster) by up to 60% when the supply of magnesium is significant reduced.
There is a direct correlation between magnesium deficiencies in rats and reduced immune defense against allergic reactions and cancers, in particular leukaemia and lymphomas."
http://www.1stvitality.co.uk/az/magnesium/
The above website has changed, so go to this pubmed abstract instead:
Proc Soc Exp Biol Med. 1975 Mar;148(3):620-4.
The effect of magnesium deficiency in mice on serum immunoglobulin concentrations and antibody plaque-forming cells.
Elin RJ.
Therefore, magnesium deficiency has profound immunosuppressive capabilities in mice by significantly reducing the number of antibody synthesizing cells and serum immunoglobulin concentrations.
PMID: 1093189
And our NK cells NEED Ca and Mg to work also:
Antibody Dependent Killer (K) and Natural Killer (NK) cells (ASCC) kill by extracellular cytotoxicity by binding to a target cell and secreting cytolysins which unidirectionally kill the target cell. Once the target is bound by an NKAR and no NKIR is activated, the cytotoxic reaction occurs.
The interaction of cell adhesion molecules between NK and the target cell may tighten the attachment. The first step is a MAGNESIUM DEPENDENT movement of the cytoplasmix organelles (Golgi and granules) of the NK cell to face the target cell. The secretion of the granule contents into the intercellular space is a CALCIUM DEPENDENT step that results in the preferential insertion of perforin pores into the target cell membrane.
http://www.microimm.mcgill.ca/coursenotes/513NKILL-Note.pdf
The above link does not work anymore. However, since these are ``course notes'', I will assume this is ``common knowledge'' at the college level for those studying microbiology/immunology.
I was merely pointing out that this is a THEORY (Putative/Supposed) presented by Marshall, not a fact that has been proven in either a dish or in a human.
Wondering if we are blocking the wrong thing...instead of blocking the PRO inflammatory cytokine, TNF alpha, is this cytokine the problem:
Inhibition of interleukin-17 prevents the development of arthritis in vaccinated mice challenged with Borrelia burgdorferi.
Burchill MA, Nardelli DT, England DM, DeCoster DJ, Christopherson JA, Callister SM, Schell RF.
Wisconsin State Laboratory of Hygiene, University of Wisconsin, Madison 53706, USA.
We showed that Borrelia burgdorferi-vaccinated interferon gamma-deficient (IFN-gamma(0)) mice challenged with the Lyme spirochete developed a prominent chronic severe destructive osteoarthropathy.
The immune response underlying the development of the severe destructive arthritis involves interleukin-17 (IL-17).
Treatment of vaccinated IFN-gamma(0) mice challenged with B. burgdorferi with anti-IL-17 antibody delayed the onset of swelling of the hind paws but, more importantly, inhibited the development of arthritis.
Histopathologic examination confirmed that treatment with anti-IL-17 antibody prevented the destructive arthropathy seen in vaccinated and challenged IFN-gamma(0) mice.
Similar preventive results were obtained when vaccinated and challenged IFN-gamma(0) mice were treated with anti-IL-17 receptor antibody or sequentially with anti-IL-17 antibody followed by anti-IL-17 receptor antibody.
By contrast, treatment of vaccinated and challenged IFN-gamma(0) mice with recombinant IL-17 (rIL-17) did not alter the development and progression of arthritis found in vaccinated and challenged IFN-gamma(0) mice without treatment with rIL-17.
Therapeutic intervention may be a realistic approach to prevent arthritis, especially if IL-17 is involved in the perpetuation of chronic or intermittent arthritis.
PMID: 12761128
[This message has been edited by Marnie (edited 12 May 2004).]
Its theory not proven the fellow is quoting from all over the internet slappin it together and saying it (AS A MATTER OF FACT). Its his theory if its good or bad that is yet to be seen for sure.
But Ill tell you this Iam not a guinea pig.
Main Entry: guinea pig
Function: noun
1 : a small stout-bodied short-eared tailless domesticated rodent (Cavia porcellus) often kept as a pet and widely used in biological research -- called also cavy
2 : a subject of research, experimentation, or testing
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Do unto others as you would have them do unto you.
But they all work independently...they all are only focused on a narrow piece of the puzzle...and they all have a piece to complete the puzzle.
"The greatest crisis facing us is a crisis in the organization and accessibility of human knowledge. We own an enormous `encyclopedia' which isn't even arranged alphabetically. Our `file cards' are spilled on the floor. The answers we want may be buried in the heap."
-Robert Heinlein
Let's try to keep this topic about Marshall's recent paper. Otherwise, it gets too confusing to lots of folks who have Lyme brain fog to follow what we are talking about.
If you'll delete your remarks about magnesium, please, then I'll go back and edit mine, too. I'm sure that others would appreciate this courtesy on our parts.
Everything about Lyme is theory, even long-term abx's. You're a guinea pig, I'm a guinea pig, we all are guinea pigs.
quote:
Originally posted by kaos:
Treepatrol,Everything about Lyme is theory, even long-term abx's. You're a guinea pig, I'm a guinea pig, we all are guinea pigs.
Maybe but at least these theories are by people in the appropiate fields of association.
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Do unto others as you would have them do unto you.
Immunologists don't have much to offer me, in my experience, and I have a decreasing IGM serum, as well as problems with Immune Complexes, both of which have been acqired and I haven't much info on what or why..
It's quite possible I'm missing something, but I do see a connection in these postings and relevance to what we're looking at.
Maybe it would be a good idea to have another thread running with discussion on the imbalances and looking at different ways to consider modulating, freeing up our powerful immune system.
Mo