GMO Spike Protein carries E coli Endotoxin and enhances Inflammatory Damage to Jabbees
Pfizer mRNA jabs are known to be contaminated with E. coli Endotoxin which finds a binding site inside the synthetic GMO Spike Protein, enhancing Inflammation
A very useful paper by Petruk et al. published in December 2020 assists greatly in understanding the structures and toxicity of E. coli Endotoxins, also known as LPS (LipoPolySaccharides) from the surface of the bacteria cells and the “smaller” fragments, known as “Lipid A” that break off when the cells are disrupted.1
Acute Respiratory Distress Syndrome (ARDS) due to Endotoxins is enhanced by Spike Protein. ARDS is one manifestation of Systemic Inflammatory Reaction common for many disease states, such as Pneumonia, severe infection, Sepsis, and burns.
Petruk et al. also reviewed key research that shows ARDS involves activation of Toll-Like receptors (TLR), such as TLR4 via Endotoxin (Lipopolysaccharide, LPS) stimulation, inducing initial systemic proinflammatory phase characterized by a massive release of Cytokines, acute phase proteins, and Reactive Oxygen Species. This is followed by activation of proteolytic cascades including the Coagulation and Complement system.
Links between picogram levels of Endotoxins from E. coli and Covid19 are provided, covering diseases including Metabolic Syndrome, Chronic Obstructive Pulmonary Disease (COPD), Inflammatory Bowel Syndrome (IBD), Kawasaki Disease and Periodontitis.
Healthy Human blood from donors was fractionated to study LPS interactions with different cell types including Peripheral Blood Mononuclear Cells. THP-1, human leukemia monocytic cell line was also studied where S protein, when combined with low levels of LPS, boosted nuclear factor-kappa B (NF-κB) activation.
They used a remarkable array of high-end science to reveal the enhancement of the Endotoxin inflammatory response caused by the SARS-Cov Spike Protein.
Ultra-low levels of Endotoxin LPS, 50 picogram/ml, showed boosted Tumor Necrosis Factor alpha (TNF-α), Interleukin-6, Interleukin-8 levels. This expected from the known Epigenetic effects of the E. coli Endotoxins.2
They used Western Blotting to show very large molecules, over 1,000,000 Daltons in weight, can be identified and separated. They estimated the molecular weight of their Spike Protein to be ∼180‒200 kDa, higher than the predicted molecular weight of 134.6 kDa, compatible with the expected increased mass due to glycosylation.
Figure 2 of Petruk et al. study shows with atomic resolution how LPS (orange) and its fragment Lipid A can hitch a ride with Spike Protein, close to the Furin Cleavage site inserted by US Bioweapons researchers3 to make the Coronavirus more transmissive and more lethal. Interaction with specific Spike residues in nanometres was calculated with Root Mean Square Deviation (RMSD). This was achieved with Transmission Electron Microscopy and Uranium staining.
Figure 6 from the Petruk et al. study reveals that multiple LPS aggregates can bind with a single or multiple units of Spike. Note the interaction with Toll-Like Receptors 4 (TLR4) and the accessory protein MD2, also known as Lymphocyte Antigen 96, LY96. At low Spike Protein concentrations, some LPS molecules bind to them resulting in disaggregation of the LPS aggregates. Free LPS molecules then bind to the known Human Endotoxin receptor, CD14, before being transferred to the TLR4/MD2 complex, which activates downstream signaling. At high Spike Protein concentrations, most LPS molecules are bound to the Spike Protein, forming large aggregates.
Petruk et al. also performed in vivo inflammation imaging of NF-κB in BALB/c Tg(NF-κB-RE-luc)-Xen reporter mice, using LPS alone or in combination with SARS-CoV-2 S protein (S) subcutaneously deposited on their backs. Noninvasive in vivo bioimaging of NF-κB reporter gene expression was performed using an In Vivo Imaging System.
Samsudin and coworkers showed that Endotoxin micelles can be disaggregated by interaction with Spike Protein and “hide” in pockets.4
The Endotoxin can be transferred to CD14 and enhance inflammation via interaction with Toll-Like Receptor 4 (TLR4).
Samsudin et al. therefore extendend important earlier work by Cinquegrani and coworkers who showed that Covid19 Spike Protein is not inflammatory toward Human Macrophages, but commercially available Spike was commonly contaminated with Endotoxin.5 Cinquegrani et al. did not consider the most potent small fragment of Endotoxin known as Lipid A.
Endotoxin used as Adjuvant in RNA jabs
The extreme toxicity6 of Endotoxins from E. coli is seen as an advantage to those who seek to profit from Covid19 and other jabs.7
E. coli Endotoxin Lipid A with a molecular weight of 1,798.4, a dodecanoate ester and a tetradecanoate ester is well described along with numerous other toxic molecules derived from bacteria cell walls.8
Update 23 May 2023
I have been alerted to a very nice article on this subject posted before I joined Substack which discussed the synergistic interactions of Spike with Endotoxin in some detail.9
Petruk G, et al. 2020. SARS-CoV-2 spike protein binds to bacterial lipopolysaccharide and boosts proinflammatory activity. https://academic.oup.com/jmcb/article/12/12/916/6028992
Samsudin F, et al. 2022. SARS-CoV-2 spike protein as a bacterial lipopolysaccharide delivery system in an overzealous inflammatory cascade. https://academic.oup.com/jmcb/article/14/9/mjac058/6761401
Cinquegrani G, et al. 2022. SARS-CoV-2 Spike protein is not pro-inflammatory in human primary macrophages: endotoxin contamination and lack of protein glycosylation as possible confounders. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8749924/
Ding D, et al. 2023. Self-Adjuvanting Protein Vaccine Conjugated with a Novel Synthetic TLR4 Agonist on Virus-Like Liposome Induces Potent Immunity against SARS-CoV-2. https://pubmed.ncbi.nlm.nih.gov/36625758/
https://pubchem.ncbi.nlm.nih.gov/compound/lipid-A
Can LPS induce IgE sensitisation to subsequent exposures to LPS?
I fear that big pharma is a lot more devious than most maybe considering. After reading a 2020 worldwide study showing a correlation between flu vaccines and Covid-19 deaths, I kept this in the back of my mind and have been researching ever since. I'm also suspecting vaccine shedding as a transmission mechanism. My theory is partly based on the 1918 Ft. Riley, KS flu pandemic which was caused by the experimental vaccines given to new recruits at induction into the military and (possibly) spread around the world via vaccine shedding. The childhood vaccines are obviously causing diseases, like autism like symptoms at epidemic levels. As was highly publicized, worldwide, more kids are now getting polio from the vaccines then from the wild. We've known since a 1980s study, that it was bacterial pneumonias that everyone died from in 1918, the very pathogens in the experimental vaccines. I'm thinking they experimented with several pathogens. I've found two bacteria that were in the vaccines, but I'm suspecting more. I haven't been able to find a verifiable source for these. The two I found appear in several sources, so I think, they're most likely were in the vaccines. Even the damn Tetanus shot has several bacteria in them. Even if you go to WWI in Wikipedia, you find that more military personnel died in non-combat then at the hand of the enemy. It was so bad, Commanders were having a difficult time finding healthy men to ship overseas, with many even getting sick on the transport ships and when the arrived. Just a theory but I am having a difficult time disproving it. Pneumococci and streptococci were the bacteria I found to have been in the experimental vaccines. Dr. Anthony Fraudci in a study he co-authored, tried to say it was a virus that induced the bacterial pneumonia and deaths. Was he trying to deflect from the potential vaccine injury narrative?