cGAS STING Interactions and Written Work
Part Three
All of these threads, and everything contained here, are a published work on Substack, and copyrighted, and protected under the Digital Millennium Copyright Act (DMCA). I do not give consent for the use of or republication of this material, under any format.
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THE GUT MICROBIOME, and COVID:
The microbiota in your gut is responsible for peripheral cGAS-STING activation, promoting resistance to systemic viral infections like COVID.
If you give an antibiotic during a viral infection, you risk inactivation of cGAS STING to deal with that viral infection, systemically.
Your gut microbiome is not some lone ranger just hanging out.
Drinking, smoking, AND specific antibiotic use, will knock down numbers of bifidobacteria (some antibiotics, even one course will reduce for A YEAR).
THIS is why changes in the gut microbiome are correlated to higher disease outcomes in people with COVID.
The cGAS STING pathway was not fully functioning due to disruptions in the gut.
Now, in the studies done by people who wrote about the gut microbiome and covid, where is your data on your participants who:
DRINK
SMOKE
USE DRUGS
ANTIBIOTIC USE?
THEY never checked. They never accounted for people who drink, smoke, use drugs, or have used antibiotics in the last year.
cell.com/immunity/fullt…
2/ The people who ran the studies on covid and the microbiome, never showed data on those who have used antibiotics, especially in the last year.
Amoxicillin
Doxycycline
Azithromycin
These things impact your cGAS STING pathway, and not in a good way.
Antibiotics are very helpful, WHEN NEEDED.
However, more than one of these reduces bifidobacteria and other species, for up to a year in the gut.
Therefore, you just fecked your cGAS STING,
christiegrace.substack.com/p/the-effects-…
The Effects of Specific Antibiotics on Bifidobacterium--short and LONG TERM changes in the microbiome, especially on Bifidobacterium.Antibiotics can significantly alter the microbiome, the community of microorganisms that inhabit various parts of the body, including the gut, skin, mouth, and other mucosal surfaces.https://christiegrace.substack.com/p/the-effects-of-specific-antibiotics
3/ STUDIES: Drinking alcohol: chronic alcohol abuse is associated with significant alterations in the gut microbiota composition, including a decrease in bifidobacteria levels
Do you drink? I do not. Not a fan. I cannot metabolize booze well. I get flushed in the face and feel like garbage on a thimble full. But a lot of people do drink.
”It has been shown that alcohol not only changes the gut environment, but also modulates the composition of gut microbiota and is associated in the development of alcohol-associated diseases”
Alcohol consumption increases gram negative bacteria. This can change levels of bifidobacteria (lowering the levels). If you change your gut flora, and reduce levels of important bacteria that act on cGAS STING, you alter your body's ability to fight off infection, especially COVID.
Might be wise to rerun some study data on those with altered microbiome and COVID.
christiegrace.substack.com/p/studies-drin…
STUDIES: Drinking alcohol: chronic alcohol abuse is associated with significant alterations in the gut microbiota composition, including a decrease in bifidobacteria levelsThese posts are prepping for what is coming. If you are NOT new here, I think you know what larger Substack is on deck (did certain people forget to check confounding variables in studies?).https://christiegrace.substack.com/p/studies-drinking-alcohol-chronic
4/ Do you SMOKE? Smoking of the cigs? The ganja?
SMOKING alters the gut microbiome--lowering levels of multiple bacteria, including Bifidobacterium
Was study data collected on people who smoke, and have worsening outcomes of COVID?
Do you drink and smoke?
“cigarette smoke changes caecal levels of certain organic acids, the population of Bifidobacterium and the pH in caecal contents of rats”
Changing the gut microbiome via smoking, can have an impact on cGAS STING.
WHERE is the data, on your particiapants who:
DRINK
SMOKE
USE DRUGS
USE ANTIBIOTICS?
christiegrace.substack.com/p/smoking-alte…
SMOKING alters the gut microbiome--lowering levels of multiple bacteria, including BifidobacteriumOver one billion people worldwide smoke dailyhttps://christiegrace.substack.com/p/smoking-alters-the-gut-microbiome
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here's a lot of talk right now about P53 and cancer. This is a lot of science for 4 AM. P53 degrades DNA exonuclease TREX1 via TRIM24, causing cytosolic dsDNA accumulation thus, triggering cGAS STING. Loss of cGAS STNIG activation means loss of tumor suppression. Right now, there is a small molecule that should hit the market (probably in three years give or take), that has nothing to do with a gene, that goes right in, and acts on STING, regressing colon cancer tumors from 70-90%. Not only that, these scientists found if they introduce it early enough, it works on colon cancer even better than that. Even more interesting, a different group of scientists took this SAME small molecule, and applied it to COVID and it's action on STING, and they found it stopped COVID disease in its tracks. Additionally, in autoimmune disease, cGAS STING is also activated, and if you come in and hit STING (in the cGAS STING pathway), you disrupt the positive feedback loop cascade that keeps autoimmune attack going. Imagine knocking out colon cancer and disease from COVID at the same time. Same with neurodegeneration--cGAS STING. There's also a reason why some autoimmune disorders hit people later in life. cGAS STING is also implicated and has been found in vivo to drive neuroinflammation in the brain, and neurodegenerative disease.
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GAS STING is the primary pathway for many of the harms caused by the
(outside of the genomic integration concern) I've got breakdowns in this thread with a mega sub stack with all one could want on how this is involved with so many of the harms being seen. https://pubmed.ncbi.nlm.nih.gov/38378748/?utm_source=substack&utm_medium=email
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cGAS STING!!!
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cGAS STING Pathway Activation by DNA Plasmid Contamination, SPIKE, and LPS in modRNA "vaccines": AIDP, Myocarditis, Stroke, Aortic Dissection, and More: Overview, and Biopsy Methods for Detection.
When DNA integration testing fails to produce results, this pathway, should.
2/ This substack breaks down the pathway in more detail, different ways it can be activated, how these are linked to not just the mRNA "vaccines", but also, how this may be the pathway involved in traditional vaccines, and how to test tissues thoroughly.
christiegrace.substack.com/p/cgas-sting-p…
cGAS STING Pathway activation by DNA Plasmid Contamination, SPIKE, and LPS in modRNA "vaccines": AIDP, Myocarditis, Stroke, Aortic Dissection, and More: Overview, and Biopsy Methods for Detection.SUPER cGAS STING SUBSTACK: Detection methods for scientists/pathologists towards the endhttps://christiegrace.substack.com/p/cgas-sting-pathway-activation-by
3/ The lipid nanoparticle has a net charge on it, and a different charge, called zeta potential. This is the charge of kinetic potential. It changes and is determined by several factors. Interaction with the LNP in conjunction with different parts in the body=different zeta.
4/ A highly negative zeta potential (LNP) can lead to clots, and it can transfect and enter the cardiomyocyte--an LNP with a neutral charge cannot do this as easily. A positive zeta potential causes "tropism" (targeting) of the lungs, causing massive clots (studies prove this).
5/ When it comes to sustained activation of the immune system, (positive feedback loop), if in the heart, nerves, lining of the blood vessels, other specific organs, brain--pick your organ or place--if cGAS STING is present, then injury with a "forever on switch" is possible.
6/ Highlights (see stack for full info): cGAS is an alarm system for your body. it protects you. It can sense, like a smoke detector, bacteria, viruses, and DNA--it "sees" it in the cells and activates (conformational changes occur). Multiple cascades occur, and the immune
7/ system is recruited--like a sprinkler system in a building responding to smoke. But, when the sprinkler system hits parts inside the building, it causes damage. And the same goes with the immune system.
Different parts of the immune system are recruited to the area. This is
8/ a normal part of our bodies--it is supposed to do this, to deal with infection. cGAS is expressed in most cell types, including immune cells, epithelial cells, and fibroblasts, whereas STING is predominantly expressed in immune cells but can also be found in non-immune cells.
9/ cGAS STING are primarily found in the cytoplasm. This is the liquid type area that is outside of the nucleus, but still in the cell space. cGAS is a cytosolic DNA sensor that recognizes double-stranded DNA (dsDNA) derived from pathogens, damaged cells, or cellular debris.
10/ When this signaling cascade occurs, in some instances, unfortunately, depending on the person, their immune system (existing autoimmune), genetics, and other factors (hyper immune activation), can do damage to the extent, the cells in the impacted area are
11/ so damaged, the nucleus inside of the cells in the area start to leak out their own DNA.
This self-DNA can further activate the cGAS-STING pathway in neighboring cells or immune cells, perpetuating the immune response.
12/ Positive Feedback Loop:
The release of self-DNA and continued activation of the cGAS-STING pathway create a positive feedback loop, amplifying the immune response and sustaining inflammation.
This amplification mechanism can contribute to
13/ chronic inflammation and autoimmune diseases if dysregulated, including MS, AIDP, Sjögren's Syndrome, Myocarditis, and more.
The immune system may recognize self-DNA as foreign or aberrant, leading to an autoimmune response
14/ against host tissues. Immune cells, particularly T cells and autoantibodies, may target self-DNA and contribute to tissue damage in autoimmune diseases such as lupus, arthritis, or inflammatory bowel disease.
15/ The FEEDBACK LOOP: HOW the cGAS STING PATHWAY IS MAINTAINED IN THE “ON” POSITION—CONSTANT INFLAMMATION, AUTOIMMUNE ATTACK, AND WORSENING OF CONDITIONS EVEN IF THERE IS NO LONGER A PRESENCE OF PLASMID DNA, SPIKE PROTEIN, OR LPS:
16/ Upon activation, the cGAS-STING pathway triggers the production of type I interferons (IFNs) and other inflammatory cytokines, which in turn promote the expression of interferon-stimulated genes (ISGs).
Some ISGs encode proteins that directly amplify the
17/ cGAS-STING signaling pathway or modulate its activity, creating a positive feedback loop that reinforces immune responses.
This pathway then goes into hyperdrive, and once this switch is flipped in this manner, it is not something that can easily be turned back
18/ to the OFF position.
Epigenetic changes induced by chronic inflammation or cellular stress can contribute to the persistence of immune activation and the development of autoimmune phenotypes.
19/ Accumulation of damaged cellular components and reactive oxygen species (ROS) contributes to tissue injury and inflammation, perpetuating immune activation and exacerbating tissue damage.
Loss of "self-tolerance" may then occur, and the body now recognizes
20/ that area or tissue type, or organ, as an invader.
The cGAS-STING pathway plays a critical role in the detection of tumor-derived DNA and the activation of anti-tumor immune responses. If this pathway gets dysregulated, you are in trouble.
21/ In addition to direct activation by exogenous DNA, the cGAS-STING pathway can also be stimulated by secondary signals released during tissue damage, inflammation, or infection, amplifying immune responses initiated by exogenous DNA and sustain pathway activation over time.
22/ Activation of the cGAS-STING pathway by DNA or self-DNA released during tissue damage may contribute to immune activation and inflammation in myocarditis, neurodegeneration, rupture of aorta, AIDP, CIDP, MS, stroke, vasculitis, small fiber neuropathy, and many other concerns
23/ Histological Examination:
If you scroll to the end of the stack, their are multiple pages and steps for determining cGAS STING activation by looking for nuclear DNA, exogenous DNA, binding to specific proteins, and more.
24/ DNA plasmid contamination with integration is only one aspect of the process. Tissues may not reveal this (if DNA has degraded and not integrated).
One would hope, the scientists/researchers right now working diligently would check this pathway for activation in
25/ tissue samples from those who have been injured, and those who have died, from exposure to mRNA COVID "vaccines".
Relying on DNA integration testing alone, is incomplete, and it is vital this testing is included in the analysis. Substack has complete mechanism and citations
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All the same pathway--myocarditis, stroke, rapid aortic dissection, neurodegenration, autoimmune demylenating polyneuropathy, fbirosis, RA, IBD, and other disorders: cGAS STING pathway. The DNA plasmid contamination and SPIKE can activate and send into a feedback loop.
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Super stack on how a positive feedback loop is generated by the
: cGAS STING Pathway activation by DNA Plasmid Contamination, SPIKE, and LPS in modRNA "vaccines": AIDP, Myocarditis, Stroke, Aortic Dissection, and More: Overview, and Biopsy Methods for Detection. https://christiegrace.substack.com/p/cgas-sting-pathway-activation-by
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Recognition of DNA by cGAS is dependent on DNA length. Double-stranded DNA (dsDNA) longer than 20 bp activates cGAS, inducing dimerization of cGAS and resulting in the formation of a 2:2 DNA/cGAS complex, whereas dsDNA less than 20 bp is not able to induce cGAS dimerization and activation" The DNA plasmid contamination in the LNP is dsDNA. The average piece of dsDNA plasmid that exists as contamination inside the RNA "vaccines" are approximately 100-120 base pair in length. ". cGAS recognizes pathogenic DNA from DNA and RNA viruses, activating innate immune cells and inducing essential immune responses against infection (Sun et al. 2013). cGAS is activated by host DNA, including nuclear, mitochondrial, and oxidized DNA" Activation of cGAs STING pathway is involved in multiple diseases including but not limited to: Autoimmune Disorders and Inflammation Stroke Aortic Dissection Thyroid Disorders Cancer https://link.springer.com/article/10.1007/s12272-023-01452-3… https://ncbi.nlm.nih.gov/pmc/articles/PMC10487967/
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inhibition of cGAS in Paraventricular Nucleus Attenuates Hypertensive Heart Injury Via Regulating Microglial Autophagy" The cGAS STING pathway is activated by exogenous (from the outside) ds(double stranded) DNA. DNA plasmid contamination is exogenous DNA. https://link.springer.com/article/10.1007/s12035-022-02994-1
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Autoimmune diseases can be triggered by abnormal activation of the cGAS STING pathway. There are options to inhibit the cGAS STING pathway. The cGAS STING pathway is activated by exogenous DNA. Plasmid DNA contamination in RNA "vaccines" is, considered to our cells, to be exogenous (from the outside) DNA. "Meloxicam inhibits STING phosphorylation and alleviates intracellular DNA-mediated autoimmune responses" "Cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway is critical for cytosolic DNA-sensing and the subsequent immune responses. The inappropriate activation of this pathway leads to DNA-induced autoimmune response. https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-023-01025-3
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"Inhibition of cGAS in Paraventricular Nucleus Attenuates Hypertensive Heart Injury Via Regulating Microglial Autophagy" The cGAS STING pathway is activated by exogenous (from the outside) ds(double stranded) DNA. DNA plasmid contamination is exogenous DNA. https://link.springer.com/article/10.1007/s12035-022-02994-1
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Activin A alleviates neuronal injury through inhibiting cGAS-STING-mediated autophagy in mice with ischemic stroke dsDNA is exogenous DNA. Plasmid DNA contamination in covid RNA vaccines is exogenous DNA. Exogenous DNA activates the cGAS STING pathway in cells. My hypothesis is, that to inhibit this pathway, might be the key to help MANY vaccine injured. I believe the current protocols used by certain groups of people to be inefficient. https://ncbi.nlm.nih.gov/pmc/articles/PMC10108189/
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cGAS inhibition alleviates Alu RNA-induced immune responses and cytotoxicity in retinal pigmented epithelium" If DNA plasmid contamination in RNA vaccines interacts with the cGAS STINg pathway, causing the immune system to become activated, attack the area, cause a domino effect and cascade where the cells release their own DNA because they are inflamed, and then the immune system attacks back, causing damage, causing a cyclic cycle of non stop damage, one might consider the avenue of inhibiting this pathway and, the potential, that doing so, WOULD STOP IT IN ITS TRACKS. https://cellandbioscience.biomedcentral.com/articles/10.1186/s13578-022-00854-y
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Inhibition of the cGAS-STING Pathway Attenuates Lung Ischemia/Reperfusion Injury via Regulating Endoplasmic Reticulum Stress in Alveolar Epithelial Type II Cells of Rats If the cGAS STING pathway is being activated by DNA plasmid contamination ni the RNA "vaccines" causing damage, one might consider treating that instead of using special mushrooms and soy that is listed in a current "protocol" https://pubmed.ncbi.nlm.nih.gov/36091334/
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"Inhibition of cGAS-STING by JQ1 alleviates oxidative stress-induced retina inflammation and degeneration" If DNA plasmid pieces are entering the cells causing a cascade effect with the cGAS STING pathway, then one might take a chance and treat this pathway in the vaccine injured, instead of , "the current protocol". https://nature.com/articles/s41418-022-00967-4
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"Inhibition of cGAS–STING pathway alleviates neuroinflammation-induced retinal ganglion cell death after ischemia/reperfusion injury" ds DNA plasmid contamination in the RNA vaccines may be interacting with the cGAS STING path. https://nature.com/articles/s41419-023-06140-0…
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Hey Medical Docs--There is a clinical trial on cGAS STING with IBS in kids correlating exogenous DNA--right now. cGAS STING pathway activation by pieces of DNA that do not belong, Maybe for vaxx injured, target it as last resort? https://sciencedirect.com/science/article/abs/pii/S0146280623006060#:~:text=The%20cGAS%2DSTING%20signalling%20pathway%20can%20impact%20the%20onset%20and,autophagy%20promotion%2C%20and%20ageing%20promotion….
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Also, zeta potential with its impact on biodistribution, the specific molar ratio required to transfect the cardiomyocyte, the charge causing clots, remodeling the inside of the blood vessels, and the DNA plasmid causing activation of cGAS STING pathway and it's impact on so many organ systems, not to mention the cancer implications and how it satisfies the muti hit cancer theory, progressing cancer--it really blows the IgG4 concern out of the water, but don't worry, you'll get on board soon.
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Spike protein activates the Sting pathway. DNA plasmid contamination should be activating the cGAS Sting pathway as exogenous DNA. Schedule allowing, I'm going to draw a unifying mega mind map pathway for the cGAS sting pathway, and all the things it's been activating. Outside of clotting and the zeta potential, this might be the main, unifying pathway. In research studies it is implicated in cancer, aortic dissection, autoimmune disorders including multiple sclerosis, auto-inflammatory, strokes, and other damage all over the body. It's implicated in ALS and dementia. Recently I found studies implicating it in nerve palsy and vocal palsy where the cause of the palsy is not damage to the nerve itself, but the inflammation of the adjacent vessel pressing on said nerve. In a nutshell which is described in detail and the other threads I've created, the presence of double stranded plasmid DNA activates the cGAS Sting pathway. This generates an immune response where cytokines and other immune cells come into the area and inflame the tissue in which the plasmid DNA is, and other immune cells come into the area and inflame the tissue in which the plasmid DNA is activating this pathway. As a result this tissue can release its own human DNA because the cells have been damaged and inflamed by the initial activation of the Sting pathway. This causes the immune system to come back again harder and stronger and cause necrosis and tissue damage. In the heart if the cardiomyocyte is transfected if the molar ratio of positively charged lipids to nucleic acids is 10 to 1, then you'd have the cardiomyocyte transfected, the cells would detect the DS DNA as well as the Spike protein. Since both of these seem to activate the cGAS Sting pathway you would be having a double whammy would you not? Just for reference they are making people take a vaccine with this Spike protein that seems to activate this same pathway. One would think it's doing it to a lesser degree and perhaps it is the combination of the DSDNA plasmid contamination with the spike protein that pushes it over the edge in some instances where the DSDNA plasmid contamination is higher as the batches are not the same for the vaccines. Earlier tweets made show studies that certain amounts or variable sizes of the DNA plasmid will activate this Sting pathway and myself and Dr Buckhaults discussed on Twitter if the contamination was sufficient to drive the activation of this pathway. However if you've got spike protein in addition to that, that might do it. This should be the main pathway for information in addition to the spike. Sting pathway recognizes it. https://pubmed.ncbi.nlm.nih.gov/35412852/
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"Activation of cGAS-STING Pathway Is Associated with MSI-H Stage IV Colorectal Cancer (dsDNA activates the cGAS-STING. Plasmid DNA IS dsDNA) Forty-one biopsy samples from metastatic CRC patients were collected at the Department of Pathology, Split University Hospital, Split, Croatia from January 2020 to December 2021. 21 patients with microsatellite unstable tumours (MSI-H) and 20 patients with microsatellite stable tumours (MSS) were randomly included in the study. Immunohistochemical staining was performed on formalin-fixed, paraffin-embedded representative tissue sections of 5 µm thickness. Recent research has revealed that STING plays a role in carcinogenesis After adjusting for age, sex, and STING expression, increased cGAS expression remained significantly associated with MSI-H colon cancer in the multiple logistic regression model (β = 1.588, SE = ±0.799, p = 0.047). https://ncbi.nlm.nih.gov/pmc/articles/PMC9818394/
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Nerve pain, chronic peripheral neuropathic pain, chronic central neuropathic pain, and inflammation can be caused by exogenous dsDNA interacting with the cGAS-STING pathway, resulting in a chain reaction.
Plasmid DNA contamination in the RNA vaccines IS dsDNA.
Unroll available on Thread Reader
2/ "The bidirectional roles of the cGAS-STING pathway in pain processing: Cellular and molecular mechanisms"
doi.org/10.1016/j.biop…
sciencedirect.com/science/articl…
https://doi.org/10.1016/j.biopha.2023.114869
3/ RNA vaccines contain plasmid dna contamination. This is ds DNA (double stranded DNA). These pieces are occurring around 200 billion per shot, and if 43 million LNP exist in one shot, roughly 4k 120 average base pair pices of DNA plasmid if evenly distributed are in each LNP.
4/ cGAS-STING pathway is a sensor of dsDNA, playing a role in cellular responses to DNA damage and viral infections.
Donnelly et al. observed l injection of STING agonists into naïve mice induced dose-dependent anti-nociception and elevated mechanical sensory thresholds.
5/ The cGAS-STING pathway is aberrantly activated in peripheral neuropathic pain.
In spared nerve injury (SNI) rats, the expression of cGAS and STING is significantly elevated in neurons and microglia of the spinal cord.
These are activated by dsDNA, locally.
6/ dsDNA-induced activation of the STING pathway is implicated in the development of neuropathic pain.
The GREAT news is, In sciatic nerve chronic constriction injury (CCI), STING agonists relieve mechanical and cold allodynia-- anti-nociceptive effect.
(we might have an "out")
7/ The bidirectional role of STING in peripheral neuropathic pain involves both pro-nociception and anti-nociception.
Pro-nociception facilitates perception of pain. contributes to sensitization of nociceptive pathways,
8/ making people more sensitive to pain involving pro-inflammatory mediators, activation of pain-sensing neurons, and circuits that transmit pain signals to the brain. Inflammation, injury, or certain pathological conditions can trigger
9/ pro-nociceptive processes, leading to increased pain.
Anti-nociceptive processes suppress or inhibit the perception of pain.
Chronic central neuropathic pain, such as that developing from spinal cord injury (SCI), involves upregulation of STING.
10/ STING knockout rescues neuronal damage after SCI, while STING overexpression increases neuronal cell death.
Aberrant activation of the cGAS-STING pathway is a major factor in SCI-induced hyperalgesia.
Hyperalgesia is a heightened sensitivity to pain,
11/ Inflammatory pain involves the release of pro-inflammatory cytokines after tissue damage.
The cGAS-STING pathway is significantly upregulated in diverse inflammatory diseases, including osteoarthritis and low back pain.
12/ STING activation in nociceptive neurons induces neuroinflammation and pro-nociceptive effects.
This means if dsDNA were to enter areas with neurons or other parts of the body with nerves, one might expect inflammation and pain in brain and nervous system.
13/ ***STING agonists can suppress nociceptor excitability and synaptic transmission, showing anti-nociceptive effects.
14/ Microglial M1-polarization, facilitated by cGAS-STING activation, contributes to hyperalgesia.
Inhibition of cGAS-STING signaling suppresses microglial M1 polarization and alleviates pain-like behaviors.
(Microglia are immune cells in the brain)
15/ Astrocyte activation in chronic pain conditions involves cGAS-STING pathway.
Astrocytes are a type of glial cell found in the central nervous system (CNS): brain and spinal cord.
16/ cGAS-STING pathway significantly regulates macrophage polarization, inducing pro-inflammatory and anti-inflammatory states.
T cells, involved in the transition from acute to chronic pain, undergo differentiation influenced by the cGAS-STING pathway.
17/ T cell differentiation:
T cell differentiation is when naive T cells, which are undifferentiated and have not encountered antigens, undergo maturation and specialization into distinct subsets of effector or memory T cells with specific functions.
18/ T cells are lymphocyte involved in adaptive immunity, and their differentiation is critical for mounting effective immune responses.
T cells
Helper T Cells (CD4+ T Cells)--TH1 and TH2
Cytotoxic T Cells (CD8+ T Cells)
TREGS
19/ **Activation of the cGAS-STING pathway leads to the production of pro-inflammatory cytokines.
Inflammatory signals influence T cell differentiation, particularly the differentiation of CD4+ T helper cells (Th cells), by favoring
20/ specific subsets based on the nature of the inflammatory stimuli.
The cGAS-STING can promote TH1 differentiation
The cGAS-STING pathway may also influence the differentiation and function of regulatory T cells (Tregs).
21/ if aberrant activation of the cGAS-STING pathway is a contributing factor to neuropathic pain, it might be relevant to SMALL FIBER NEUROPATHY, AIDP, and CIDP.
.
ncbi.nlm.nih.gov/pmc/articles/P…
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9376357/
22/ While spike protein is expressed in areas the LNP enters, it should also benoted that dsDNA is capable in specific sizes and amounts, of activating the cGAS STING pathway.
This could set off a chain reaction.
In the simplest of terms, dsDNA that is exogenous, which enters
23/ from outside the cell, activates cGAS STING pathway, which activates immune system to rush to the area, which causes inflammation to cells/issue, and this can lead to cells releasing their OWN DNA, which lands outside of the nucleus and reactivates
24/ cGAS STING, causing a chani reaction, and catastrophic tissue damage.
In the heart, in the cardiomyocyte, this might lead to myocarditis, if the molar ratio of positive lipids to nucleic acids were 10: 1 with a strong negative zeta potential on the LNP.
25/ cGAS STING warrants exploration into neuropathic pain and damage which might be caused by the introduction of dsDNA into the area which did not start with injury, but a contamination event of plasmid DNA into cells into that local area via RNA/LNP vaccines.
Here. Knock yourself out:
@NestCommander
"Constitutively active STING causes neuroinflammation and degeneration of dopaminergic neurons in mice"
Constitutively active STING causes neuroinflammation and degeneration of dopaminergic neurons in miceConstitutive activation of an innate immunity response in mouse brain causes degeneration of dopaminergic neurons, suggesting novel targets for potentially neuroprotective strategies.https://elifesciences.org/articles/81943
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Happy new Year. Time to jump right in. Do or do not--there is no try. For the science folks: Read these two in tandem: 1: "Innate Immune Response to Cytoplasmic DNA: Mechanisms and Diseases" "Suppression of cGAS Activity" "Suppression of MITA Activity" https://annualreviews.org/doi/10.1146/annurev-immunol-070119-115052…… 2: "SARS-CoV-2 spike protein-induced cell fusion activates the cGAS-STING pathway https://pubmed.ncbi.nlm.nih.gov/35412852/ (there is no explain it to me like I am 18 version)
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LNICAL TRIALS ARE IN PROCESS ON THE HARMS OF EXOGENOUS DNA ON CHILDREN!
"Exploration of the Activity of DNA Located Outside of Cellular Nucleus to Amplify Inflammation in Inflammatory Bowel Disease in Children Through Biological Pathway Cyclic GMP-AMP Synthase (cGAS)
2/Exploration of the Activity of DNA Located Outside of Cellular Nucleus to Amplify Inflammation in Inflammatory Bowel Disease in Children Through Biological Pathway Cyclic GMP-AMP Synthase (cGAS) - Stimulator of Interferon Genes (STING) (ROXANE)
3/ ID NCT05916274
Sponsor Centre Hospitalier Régional d'Orléans
Information provided by Centre Hospitalier Régional d'Orléans (Responsible Party)
Last Update Posted 2023-06-23ClinicalTrials.gov
https://ClinicalTrials.gov
https://clinicaltrials.gov/study/NCT05916274?term=Exogenous%20DNA&rank=3
4/ "Study Overview
Brief Summary
Frequency of Inflammatory Bowel Diseases in children (IBD)-Crohn's disease (CD), Ulcerative colitis (UC) is constantly increasing. Pediatric-onset IBD represent a different nosological entity (from adult IBD) because of their
5/ major inflammatory activity, their significant anatomical extent and their stenotic and/or fistulizing character sometimes from diagnosis. Intestinal lesions are due to dysregulation of the intestinal immune system but the cause is unknown.
6/The investigators hypothesize that extranuclear DNA participates in the amplification of the inflammatory response at the intestinal and blood levels during pediatric IBD through the cGAS-STING pathway.
7/ The investigators will analyse blood and fecal samples, and colonic biopsies issued from ill children and control participants on age of 6 to 17 years. The investigators think that this study will provide a better understanding of the mechanisms involved in pediatric IBD,
8/ assess the place of the cGAS-STING pathway, identify potential biomarkers of pediatric IBD and new potential therapeutic targets based in particular on the inhibition of the cGAS-STING pathway.
9/ Extracellular and extranuclear DNA (enDNA) play a major role in innate immunity by stimulating pro-inflammatory responses and activating type I interferon production. The pro-inflammatory action of enDNA is mediated by enzyme cGAS,
10/ protein STING, toll-like receptor 9 (TLR9), and the inflammasome complex NLRP3. The investigators hypothesize that enDNA participates in the amplification of the inflammatory response at the intestinal and blood levels during pediatric IBD through the cGAS-STING pathway.
11/ They also hypothesize that there are links between the cGAS-STING pathway and other pathways involved in pediatric IBD such as NOD2 and Autophagy. The investigators will analyse blood and fecal samples,
12/ and colonic biopsies issued from ill children and controls on age of 6 to 17 years. The investigators think that this study will provide a better understanding of the mechanisms involved in pediatric IBD, assess the place of the cGAS-STING pathway,
13/ identify potential biomarkers of pediatric IBD and new potential therapeutic targets based in particular on the inhibition of the cGAS-STING pathway."
https://clinicaltrials.gov/study/NCT05916274?term=Exogenous%20DNA&rank=3
14/ (above is directly from the study--below is commentary)
The DNA plasmid contamination that has been recently discovered in the RNA vaccines is ds DNA, that is double stranded DNA. It is also exogenous. Exogenous means from outside.
15/ The DNA plasmids that were used in process TWO of what is currently, and what has been given, to over half of the Earth's population, were not filtered out properly. An old rule regarding DNA is in place that does not account for the use of an LNP--a transfection agent.
16/ Transfection is the process of artificially introducing nucleic acids (DNA or RNA) into cells.
Introduction to Transfection | Thermo Fisher Scientific - USTransfection is the process of artificially introducing nucleic acids (DNA or RNA) into cells, utilizing means other than viral infection.https://www.thermofisher.com/us/en/home/references/gibco-cell-culture-basics/transfection-basics/introduction-to-transfection.html
17/ the ds (double stranded) DNA plasmid contamination has the same type of structure of what is being studied in this clinical trial.
18/ These clinical trials (there are more) have unbelievable potential for implications regarding human exposure to exogenous DNA via contamination in vaccines.
https://archive.is/8sXsq
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