Bcl-2
Sept 11, 2024 7:49:47 GMT
Post by Admin on Sept 11, 2024 7:49:47 GMT
Why do Lyme infections cause persistent infection? There is a lot of money being given to researchers to solve that problem but it’s not really that complicated of a problem to understand.
It is pretty obvious that you only get “persistent infection” when the system is using treatments that don’t really apply to the problems that these infections cause. In reality the term “persistent infection” is interchangeable with “treatment doesn’t work”. Antibiotics don’t apply because they can’t overcome the ways that the bacteria defend against them.
Bartonella shuts down apoptosis inside the cells it infects and this will create a niche for other infections too. Bartonella is the dominant infection causing persistence and Borrelia is the co-infection.
This paper really sums up what the actual problem is;
scholarworks.gsu.edu/cgi/viewcontent.cgi?article=1068&context=biology_diss
“Bartonella Henselae Inhibits Cellular Apoptotic Regulators to Ensure Survival”
These apoptotic regulators are used by the bacteria to defend against the immune system after they make adjustments to them and by blocking these adjustments then the immune system can again kill the infected cells and start the process of eliminating the so called “persistent infection”.
So far these doctors and lyme foundations don’t talk about this aspect at all because they really don’t understand the subject matter, so let's understand the problem.
Bartonella has defense mechanisms that don’t allow conventional treatments like antibiotics or antimicrobials to work very well. Bartonella can be effectively killed by the immune system but bartonella shuts off the immune system so it can survive. Bartonella also causes cancer.
Bartonella creates immune checkpoints. These prevent the immune system from killing infected cells.
When you inhibit the blocking proteins cells can become apoptotic again.
The compounds that inhibit the proteins that stop the immune system from working are called Immune Checkpoint Inhibitors.
Solamargine is an immune checkpoint inhibitor for bartonella and something that makes it work better is fucoidan.
When you turn the immune system back on then it will kill Bartonella and the abnormal cells that bartonella creates.
Solamargine works as an immune checkpoint inhibitor and using it together with Fucoidan makes it very effective.
A considerable amount of research has been undertaken on various types of fucoidan and cancer.
B cell lymphoma protein #2 is an important protein that cancer cells use to prevent the immune system from killing the cancer cell.
www.nature.com/articles/s41419-020-03144-y
“BCL-2 family proteins play a critical role in promoting survival of tumor cells”
Bartonella also upregulates the anti-apoptotic proteins of the Bcl-2 family so the immune system can’t kill it.
pubmed.ncbi.nlm.nih.gov/16926411/
“Autocrine role for interleukin-8 in Bartonella henselae-induced angiogenesis”
“Both in vitro angiogenesis assays were IL-8 dependent. B. henselae-mediated inhibition of apoptosis, as indicated by gene expression of Bax and Bcl-2, was also shown to be IL-8 dependent in endothelial cells.”
www.ncbi.nlm.nih.gov/pmc/articles/PMC3255967/
“Intruders below the Radar: Molecular Pathogenesis of Bartonella spp.”
“Further experiments in the same study revealed a critical role of autocrine IL-8 signaling in the stimulation of endothelial cell proliferation and angiogenic phenotypes in response to B. henselae infection. The mitogenic stimulus was accompanied by a potent antiapoptotic effect via a strong increase in the ratio of Bcl-2 to Bax”
Pharma has their answer to this immune system resistance in a product called Venetoclax.
This protocol uses 2 strong natural Bcl-2 inhibitors, Solamargine and Fucoidan.
www.ncbi.nlm.nih.gov/pmc/articles/PMC5920861/
"Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells"
"In addition, western blot analysis demonstrated that solamargine inhibited the protein expression of Bcl-2"
www.ncbi.nlm.nih.gov/pmc/articles/PMC7069570/
“Fucoidan Induces Apoptosis and Inhibits Proliferation of Hepatocellular Carcinoma via the p38 MAPK/ERK and PI3K/Akt Signal Pathways”
“Fucoidan significantly promoted apoptosis of LM3 cells through a mechanism involving activation of caspases 8, 9, and 3 accompanied by changes in B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax)”
pubmed.ncbi.nlm.nih.gov/27203545/
“Fucoidan inhibits lymphangiogenesis by downregulating the expression of VEGFR3 and PROX1 in human lymphatic endothelial cells”
There are two types that have shown this activity to activate the immune system in the way it needs to be activated against bartonella. These are Fucus vesiculosus which is a brown seaweed typically found along sheltered coastlines of the Northern Hemisphere. Commonly known as bladderwrack, and Undaria pinnatifida, commonly known as wakame, which is a brown seaweed that inhabits coastal waters to depths of approximately 60 feet deep.
Bladderwrack;
www.iherb.com/pr/nature-s-way-bladderwrack-580-mg-100-vegan-capsules/1844
Wakame;
www.iherb.com/pr/life-extension-optimized-fucoidan-with-maritech-926-60-vegetarian-capsules/37817
Fucoidan is known to make other cancer treatments work better;
Bartonella creates immune checkpoints and using Solamargine blocks these checkpoints or counteracts them so the immune system will attack Bartonella. Adding Fucoidan makes this process more effective by activating NK cells and activates interferon gamma.
www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.733246/full
“Fucoidan-Supplemented Diet Potentiates Immune Checkpoint Blockage by Enhancing Antitumor Immunity”
This next link explains why immune checkpoint inhibitors are important.
bartonella.freeforums.net/thread/132/immune-checkpoint
~d