Transferrin is a blood plasma protein for iron ion delivery that, in humans, is encoded by the TF gene. Transferrin is a glycoprotein that binds iron very tightly but reversibly. Wikipedia
If I remember correctly, Bb has a transferrin gene...
Identification of a transferrin-binding protein from Borrelia burgdorferi.PMID: 8757812
"transferrin frees iron directly into the cell" Encyclop�dia Britannica
If Bb is binding to transferrin which contains sialic acid and galactose, is free iron not available to the cell?
Or is this happening? Is Bb acting like an antibody to transferrin?
"Listeria is an organism which requires iron for growth, yet *macrophage* listericidal mechanisms are also likely to be iron dependent.
(Note Bb does NOT require iron for growth.)
Antibody to transferrin, which prevents it binding its receptor, inhibits listericidal ***macrophages*** from killing this bacterium."
Calcitriol (active vitamin D) binds to intracellular vitamin D receptor (VDR), which subsequently heterodimerizes with another nuclear receptor retinoid X receptor (RXR).
Activation of Retinoid X Receptor increases dopamine cell.
So if active vitamin D cannot bind to its receptor (carbohydrate is removed from a precursor protein) then the "subsequent things" can't happen...activation of the RXR and so long dopamine?
Sick with me...
A Japanese doctor has figured out that our macrophages (think of them as pac-men gobbling up Bb) aren't working. He has figured out how to restore them.
Basically a precursor glycoprotein is "robbed" of "glyco"....simplified.
Normal Gc gobulin protein (also called vitamin D binding protein), an abundant glyco-protein found in human blood serum, becomes the molecular switch to ***activate macrophages***
when it is converted to its active form, called Gc macrophage activating factor (Gc-MAF).
This is how he figured out how to help our macrophages:
Treatment of purified Gc protein (vitamin D binding protein) with (1) beta-galactosidase and (2)sialidase generates Gc-MAF.
MAF = macrophage activating factor.
Sialidase is also called Neuraminidases and they catalyze the hydrolysis of terminal sialic acid residues.
(I'm guessing Gc = guanylate cyclase which causes GTP -> cGMP and pyrophosphate. Soluble guanylyl cyclase (sGC) is the only known receptor for NO = nitric oxide. Guanylate cyclase is dependent on Mn...which we KNOW Bb is dependent on.)
Gc-MAF isn't happening because a "glyco" is removed from a glycoprotein precursor of MAF via an immunosuppressant called
Nagalase/a-N-acetylgalactosaminidase.
Now about beta galactosidase - one of the things he treated the Gc protein with.
Lactase (or β-galactosidase) is the enzyme involved in the hydrolysis of lactose
to ***galactose*** and glucose.
It's LACTASE!
Remember...the lizard's rhodopsin contains galactose which "happens" when lactose is hydrolyzed (along with glucose produced too)via lactase/beta galactosidase.
Curiously:
Cells expressing beta-galactosidase grown in the presence of X-gal and IPTG (to induce the expression) will turn BLUE.
Is that the "blue" (chromophore) belly on the WFL...beta galactosidase -> increased galactose content in the WFL's rhodopsin?
It appears we are trying to increase galactose:
"Using IL-1-beta-galactosidase " IL1-B.
(Ongoing levels of IL1B and TNF alpha are bad...very, but I'll have to leave it at that for now.)
Now about sialidase.
Sialidase fusion protein cleaves the sialic acid RECEPTOR.
If the RECEPTOR is kapoot does this -> increased sialic acid that can't lock onto its cleaved receptor?
Oddly...the word sialic acid comes from the Greek for saliva.
Does Bb's OspC pick up sialic acid in the tick's saliva?
Apparently bacteria MAKE sialic acid:
In bacterial systems, sialic acids are biosynthesized by an aldolase enzyme. The enzyme uses a mannose derivative as a substrate, inserting three carbons from pyruvate into the resulting sialic acid structure.
Sialidase treatment ***reduced the reactivity of the SG3-1 antibody*** to α and β tubulin molecules.
I suspect Bb's Osp proteins are OspA and OspB "tubulins" = globular proteins.
You wouldn't believe what else sialidase can help!
Sialidase improves nerve regrowth, motor recovery and nervous system function. June 2010
And...
Sialidase Fusion Protein as a Novel Broad-Spectrum Inhibitor of Influenza Virus Infection
...potent antiviral and cell protective efficacies against a panel of laboratory strains and clinical isolates of *IFV A* and *IFV B,*
I cannot cut and paste the following, but go here and look for sialic acid + galactose mentioned with regard to CD22 (first page lower left):
CD22 looks to recognize Sia alpha2-6GAL (sialic acid - galactose)
Generally speaking, CD22 is a regulatory molecule that
***prevents the overactivation of the immune system and the development of autoimmune diseases.***
It would appear the sialic acid-galactose in the WFL's rhodopsin may prevent the development of autoimmune disease.
Remember sialic acid and galactose are SUGARS.
Now...Once again, the Japanese doctor treated the Gc protein with beta-galactosidase and sialidase.
This is what it does to a particular RECEPTOR:
However, treatment of membranes with sialidase and terminal β-galactosidase
further *increased the mobility of GC-C*
and this form of GC-C co-migrated with the 130 kDa form of GC-C.
Interestingly, there was no increase in the basal guanylate cyclase activity or no decrease in the ST peptide-mediated activation of GC-C after sialidase and/or galactosidase treatment (Figure 8B).
These results indicate that
the addition of sialic acid and galactose residues during the transit from the Golgi to the PM, is important for
achieving the correct folding of the ECD of GC-C, to allow repression of basal activity and a conformation that is required for ligand stimulation.
(guanylate cyclase C) = GC-C = a RECEPTOR-Guanylate Cyclase
So...would a high transferrin on a blood test mean anything according to the above info???
Posts: 236 | From Illinois | Registered: Feb 2009
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
I would assume...
Identification of a transferrin-binding protein from Borrelia burgdorferi.
PMID: 8757812
Bb present-binding to transferrin (which helps us transport iron) and need for us to make more?
In iron deficiency, the iron level is low, but the TIBC (Total iron-binding capacity) is increased, thus transferrin *saturation* becomes very low.
In iron overload states, such as hemochromatosis, the iron level will be high and the TIBC will be low or normal,
***causing the transferrin saturation to increase.***
UIBC may be ordered as an alternative to TIBC.
It is customary to test for transferrin (instead of TIBC or UIBC) when evaluating a patient's nutritional status or liver function.
Because it is made in the liver, transferrin will be low in patients with liver disease.
Transferrin levels also drop when there is not enough protein in the diet, so this test can be used to monitor nutrition.
Symptoms of iron overload will vary from person to person and tend to worsen over time. They are due to iron accumulation in the blood and tissues. Symptoms may include:
Joint pain Fatigue, weakness Lack of energy Abdominal pain Loss of sex drive Heart problems However, many people have no initial symptoms.
I remember Tincup saying she always felt better when she had to "donate" a lot of blood for testing.
She said a clear sign of babesia was to watch your RBC distribution width (on a total blood count)...i.e., watch for how far apart are the RBCs.
Because MANY pathogens use iron to replicate, there is a possibility the body goes into an "iron storage" mode (spleen).
Theoretically that might hurt the macrophages if they need iron.
Also...low levels of PFK can -> anemia. This happens to our astronauts (Skylab research a long time ago.)Also...we need Mg to MAKE OUR enzymes and Mg levels plummet at the outset of lyme.
Bb is PFK dependent. It is phosphofructokinase and is the "rate limiting" enzyme for glycolysis.
Restless leg syndrome:
With CSF examination, the iron and ferritin values were lower and the ***transferrin values were higher*** in the RLS group than those in the non-RLS group.
J. Sleep Res. (2005) 14, 43-47
I empathize...all this information makes ME dizzy and I do not have lyme.
This is such a complex disease.
[ 08-21-2010, 10:53 PM: Message edited by: Marnie ]
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Pinelady
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posted
Does this help to explain why some of us have high hemoglobins but low protein?
Do you think it is something in the saliva shutting off our innate immunity genes?
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Marnie
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posted
Ticks' saliva impacting OUR immune response...oh YES indeed. In fact they are working on a lyme vaccine based on the tick's saliva, not Bb's Osps (newbies...outer surface proteins in Bb's cell wall):
Dehydration produces falsely high hemoglobin - most common cause.
Also:
Congenital heart disease, heart failure, cor pulmonale and all other heart problems, associated with high blood pressure in the arteries of the lungs, can also increase hemoglobin levels.
Lung disease like pulmonary fibrosis, where the tissue scars or thickens between the air sacs in the lungs, also tends to increase the hemoglobin levels.
People living in high altitudes also have high levels of hemoglobin, as high altitude means lessor level of oxygen, resulting in increased production of blood cells.
Anabolic steroid used to enhance body building, can also stimulate red blood cell production.
Smoking drops the level of oxygen in the lungs, so to balance out the deficiency, the body raises levels of hemoglobin.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
Frequent Contributor (5K+ posts)
Member # 18524
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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