Circulating Spike in mRNA induced myocarditis
The endotoxin connection
Earlier today the Twitter account Dr. John B tweeted the following paper. Credit for the screenshot goes to him too.
Circulating spike protein detected in post–COVID-19 mRNA vaccine induced myocarditis:
Very early in the pandemic, when they proposed and started rolling out trials for the mRNA and published (the now factually known manipulated) data, I wrote a few observations, which got me chastised or blocked my many “experts”.
I stated that given different mechanisms, the cells producing Spike Protein were too irritant to your body’s immune system, and besides the problems with protein translation (how the cell machinery produces proteins in their proper form), I said the cells were being ripped apart and (soluble) Spike Protein was floating around.
The problem with such mechanism is the fact that the Spike Protein itself is biologically active depending on where it finds itself and the cells surrounding it, and especially as a signaling protein to start many different molecular cascades. This is a quote from a December 16, 2022 tweet.
People keep sending me this paper. Myocarditis in regards to the mRNA spike is too varied, you would need a really big autopsy sample, but infiltration will be overrepresented. Besides other aspects the real clue here is HHV-6.
I will explain the HHV-6 later it plays a role in the long-term dysfunction and damage we will see rather than short-term, sudden, abrupt damage, but I do maintain my assessment of infiltration being overrepresented. Infiltration can happen in many forms, but I do believe one overlooked one bear more weight.
The free Spike Protein is so important in this regards is simple. I often merely alluded to or don’t mention specific parts of certain papers for two reasons. One is to see if people will actually read the paper as they should, and the second is to avoid going viral, this second one also explains why I title my Substacks the way I do.
A section of the very important paper referenced above that I purposefully did not mention was about the mRNA Spike Protein, which does what is described in the paper with much more strength than viral Spike. That means, effectively, Spike Protein from mRNA will act as a stronger endotoxin “manipulator” than from the virus.
This give us the second biggest problem, as I mentioned multiple times, the Spike Protein amino acid structure itself acts as a membrane piercer, meaning the Spike Protein can pierce cells and get inside and create a reaction depending on the type of cell, but the biggest concern is a paper I left here, in a seemly unrelated substack. I will leave the important part inside a quote below.
The detection of the SARS-CoV-2 spike protein after bacterial co-incubation (Figure 6) suggests that the interaction between spike protein and S. pneumoniae likely involved direct adhesion of the S1 subunit to bacterial surface molecule(s).
From the results of this in vitro study, we propose that SARS-CoV-2 and related coronavirus infections may trigger an active dispersion of bacteria from biofilm.
The Spike Protein not only can “manipulate” LPS and deliver endotoxins and cause inflammatory cascades, but it can both pierce membranes and burst biofilms open. These 3 mechanisms together open up a lot of possibilities.
Endotoxins are known to affect both renal and cardiac function, merely a decade ago there was a novel proposal of endotoxin-induced myocarditis. Infiltration of heart tissue by exposure to Endotoxin (LPS to be specific) has been researched for the last 10 years extensively. Here is a very good example of what is going on among severe patients, and a subset of Long Covid patients.
Sustained exposure to systemic endotoxin triggers chemokine induction in the brain followed by a rapid influx of leukocytes
The entire discussion section of the paper above is worth reading, even if you are a layman, a lot of amazing information can be found there, with specific attention to this section from my own (somewhat biased) perspective.
At some point, in a somewhat significant portion of Long Covid, and people bearing all different sequelae from the viral infection (mild, moderate, or severe) this endotoxin mechanism will be the major driver of long-term changes. The biofilm interaction also plays a major and significant role, to be covered later this month.
And to drive this point further, here are two papers talking about LPS, commercially available proteins (labs buy Spike a lot of the time), and contamination.
SARS-CoV-2 Spike protein is not pro-inflammatory in human primary macrophages: endotoxin contamination and lack of protein glycosylation as possible confounders
Furthermore, we also show that the huge cytokine/chemokine production, observed in human MΦ tested with several commercially available recombinant SARS-CoV-2 Spikes, is due primarily to endotoxin (i.e., LPS) contamination of the recombinant peptides, and importantly that Spike boosts LPS-mediated pro-inflammatory action in human MΦ
Of note, despite 1 ng/ml of LPS was identified as the concentration threshold for MΦ response, we observed that even lower endotoxin levels (i.e., 3 EU/ml) of Spike were associated to inflammation, suggesting that LPS at very low concentrations did not induce inflammation per se, but only when combined to Spike, i.e. Spike can work as a cofactor of the inflammatory action of LPS. This is in accordance with a recent paper showing that SARS-CoV-2 Spike binds to bacterial LPS, leading to changes in LPS biophysical state, thus boosting its pro-inflammatory activity in monocytes and human MNCs through TLR4-NF-κB activation (Petruk et al. 2020). The proven synergy between LPS and Spike is crucial in an attempt to explain the increased risk of severe COVID-19 in conditions characterized by subclinically increased circulating levels of LPS generated by the host gut microbiome, such as metabolic syndrome, obesity, and type 2 diabetes (Cani et al. 2012; Drucker 2021), as well as provide new therapeutic targets.
Variable Induction of Pro-Inflammatory Cytokines by Commercial SARS CoV-2 Spike Protein Reagents: Potential Impacts of LPS on In Vitro Modeling and Pathogenic Mechanisms In Vivo
Moreover, commercial spike protein reagents contained varying levels of lipopolysaccharide (LPS), which correlated directly with their abilities to induce cytokine production. The LPS inhibitor, polymyxin B, blocked this cytokine induction activity. In addition, SARS CoV-2 spike protein avidly bound soluble LPS in vitro, rendering it a cytokine inducer. These results not only suggest caution in monitoring the purity of SARS CoV-2 spike protein reagents, but they indicate the possibility that interactions of SARS CoV-2 spike protein with LPS from commensal bacteria in virally infected mucosal tissues could promote pathogenic inflammatory cytokine production.
You add Galectin-3, and the Galectin mimic in the Spike and things get interesting, pretty damn fast.
As a last addendum. Ivermectin inhibits LPS-induced production of inflammatory cytokines and improves LPS-induced survival in mice. Ivermectin inhibits JNK and p38MAPK and NF-κB signal pathways.
Truly the most coincidental of ages.
Appreciate the support of everyone who chooses to support this Substack, and everyone who shares it. Thanks to each one of you.
wow, horse paste blocks LPS production of inflammatory cytokines.
Horses get all the good stuff.
COVID always seemed like a bacterial infection.