First...keep in mind, Bb has a gene (protein) called LuxS that it uses for quorum sensing, etc. and that gene needs a form of iron - an ION - Fe+2 = ferrous.
Short review (with links):
Recent research has shown that ***LuxS uses Fe(2+)*** to catalyze an internal redox reaction, shifting the ribose carbonyl group from its C1 to C3 position.
PMID: 15450491
It was noted that the LuxS gene was not consistent in its location among chromosomes,
but in one species (Borrelia burgdorferi),
LuxS was found to be at the terminal position of a three gene sequence.
Iron is transported to our cells by transferrin (a protein which is made in the liver) and attaches to a cell receptor...a transferrin receptor.
*Initially* in lyme, the transferrin receptor is upregulated on macrophages. Apparently it helps them to "recognize" Bb (Bb has a protein that locks onto transferrin.)
When and if the transferrin receptor is downregulated on macrophages, then intracellular oxidative stress goes DOWN.
(Which doesn't appear to be the case.)
Each transferrin molecule can carry two iron ions.
Inside cells, extra iron ions are locked safely in the protein shell of *ferritin*.
Protein shell with iron ions = ferritin.
After entering the ferritin (protein) shell,
iron ions are converted into the ***ferric state***, where they form small crystallites
along with phosphate and hydroxide ions.
There is room to pack about 4500 iron ions inside.
Now how does Bb go about "stealing" (our) stored iron (and phosphate?) in the ferritin protein?
Does it use iron before it can be stored in the intracellular ferritin protein as Fe+3?
Iron is stored as Fe+3 (ferric)in ferritin, but Bb's LuxS gene/protein needs Fe+2 (ferrous).
What breaks up the ferritin protein, releasing the iron (as needed) and what converts Fe+3 to Fe+2 for Bb's use?
I will provide more information regarding the LuxS gene (a protein). I've found a lot more critical information about that "quorum sensing" gene and how we might impact it.
All we may need to do is mess with one of Bb's essential proteins to impact "his" survival...hopefully.
[ 06-21-2012, 06:26 PM: Message edited by: Marnie ]
Posted by Razzle (Member # 30398) on :
I would think some enzyme would break the iron off from the ferritin protein, and another enzyme probably converts between Fe+3 and Fe+2. But I don't know what these enzymes are called.
Posted by seekhelp (Member # 15067) on :
If one has low iron confirmed through blood testing, do we continue to not take iron due to this knowledge? Can we kill Bb before we die first from iron depletion?
Posted by jwall (Member # 22999) on :
I don't understand any of the above, but both my son and I have low ferritin. We are getting IV iron infusions per my LLMD's request. Is this bad?!
Posted by seekhelp (Member # 15067) on :
We are never supposed to actually know the action needed to be taken. lol. It's like the old Choose Your Own Adventure books where you just randomly turn pages and see what happens.
Posted by Lymeorsomething (Member # 16359) on :
Thanks, Marnie. I did not realize Bb uses iron, but my ferritin has been low for a long time. Certainly, it seems like a catch-22. An optimal ferritin level is likely 80-100 and is important for thyroid function (and hair growth). However, supps may feed lyme and any intestinal overgrowth one has. Tricky at best.
I'm a heavy tea drinker which makes it even harder to put the iron back in.
Posted by terv (Member # 29410) on :
Marnie,
You said: "Bb has a protein that locks onto tranferrrin - a protein that ***transports iron into the cell***:"
and also said "In hemochromatosis iron is high, transferrin is low,"
My transferrin is much lower than the average person but at the same time my transferrin is 90% loaded with iron compared to 35% for the average person. So is the net effect good or bad for me as far as lyme?
Posted by AuntyLynn (Member # 35938) on :
Are you saying that hematochromotosis can be CAUSED by Lyme?
I have a friend that's on the standard medical merry-go-round. She tested positive for Lyme (with a LOT of symptoms), then after a second test they told her she does NOT have Lyme! (Which seems like a misinterpretation of the Western Blot to me).
They are telling her that her blood disorder is "hereditary!" I still think she has Lyme.
Posted by terv (Member # 29410) on :
I am not saying hemochromatosis is caused by lyme and neither is Marnie (I dont think).
The question I have is whether lyme is benefiting from my high TSAT%.