Endotoxin in Pfizer Jabs causes Heart Damage

Endotoxin in Pfizer jabs increases expression of MicroRNA 155 that is known to induce Heart Damage, independent of synthetic mRNA or LNPs.

As I have recently stressed, every vial of Pfizer jab contains Endotoxin arising from the manufacturing process.¹

The jabs are known to cause Heart Damage, evident from the initial trial.²

Here I will discuss a new perspective on the Mechanism of Heart Damage, independent of the mRNA or Lipid Nanoparticles in the jabs, caused by Endotoxin.

Joining the Dots

As reviewed by Cardiac specialist Dr Peter McCullough³ and co-authors, a major concern about the mRNA jabs is Innate Immune Supression.

In that review there are a number of references to upregulation of miR-155, which is found in Covid19 infected people. It is a predictor of Myocardial Damage and Inflammation independent of Covid19, as shown in a paper from 2018 that they quote.⁴

During myocardial infarction, miR-155 is sharply upregulated in macrophages in the heart muscle and released into the extracellular milieu within exosomes. These exosomes are delivered to fibroblasts, and miR-155 downregulates proteins in the fibroblasts that protect from inflammation and promote fibroblast proliferation. The resulting impairment leads to cardiac rupture.

McCullough et al. then quote another paper from 2017 by Wang et al.⁵

Wang et al, in turn quote a paper from 2007 by Tili et al. that shows that Endotoxin upregulates miR-155.⁶

A more recent review by AbdelMassih et al links miR-155 to Myocarditis after mRNA jabs.⁷

A 2016 paper showed that genetic silencing attenuates Endotoxin Induced Myocarditis.⁸

So Endotoxin, known to be in the mRNA jabs, damages Hearts directly.

Why Younger People have more Heart Damage from Jabs

AbdelMassih et al. provide the most plausible explanation for why Death from Myocarditis is more prevalent in younger people, as shown by their scheme.

Older people have less muscle mass, which can be measured by the Sarcopenia Index, and therefore generate less miR-155.

microRNA-155 Targets CD47 “Don’t Eat Me Tag”

A very interesting paper whch provides a clue to references to CD47 regarding the Adverse Events reported after the Covid19 jabs shows that the Endotoxin upregulation of miR-155 targets CD47 and angiotensin type 1 receptor to promote nitric oxide (NO)-mediated vasorelaxation and vasoplegia.⁹

We identified microRNA-155 as a highly up-regulated multifunctional mediator of sepsis-associated cardiovascular dysfunction. In humans, plasma and myocardial microRNA-155 levels correlate with sepsis-related mortality and cardiac injury, respectively, whereas in murine models, microRNA-155 deletion and pharmacologic inhibition attenuate sepsis-associated cardiovascular dysfunction and mortality. MicroRNA-155 up-regulation in septic myocardium was found to be mostly supported by microvascular endothelial cells. This promoted myocardial microvascular permeability and edema, bioenergetic deterioration, contractile dysfunction, proinflammatory, and nitric oxide-cGMP-protein kinase G signaling overactivation. In isolate cardiac microvascular endothelial cells, microRNA-155 up-regulation significantly contributes to LPS-induced proinflammatory cytokine up-regulation, leukocyte adhesion, and nitric oxide overproduction. Furthermore, we identified direct targeting of CD47 by microRNA-155 as a novel mechanism of myocardial and vascular contractile depression in sepsis, promoting microvascular endothelial cell and vascular insensitivity to thrombospondin-1–mediated inhibition of nitric oxide production and nitric oxide–mediated vasorelaxation, respectively. Additionally, microRNA-155 directly targets angiotensin type 1 receptor, decreasing vascular angiotensin II reactivity. Deletion of microRNA-155 restored angiotensin II and thrombospondin-1 vascular reactivity in LPS-exposed arterial rings.

The “don't eat me” signalling molecule CD47, which inhibits phagocytosis by binding to signal regulatory protein α on macrophages, is overexpressed in a number of Cancers.¹⁰

Endotoxin upregulating miR-155 targeting and reducing CD47 will lead to increased tissue destruction throughout the body, expressed as Auto-Immune diseases.

miR-155 Decreases Exponentially with Age

Ong et al. analyzed airway biopsy samples which showed young people have much higher miR-155 than the elderly, dramatically increasing risk of Myocarditis.¹¹

Heart is Damaged by Positive Feedback Loop

Endotoxin causes expression of IL-1β, which catalyzes expression of itself by initiating a Positive Feedback Loop.¹²

IL-1β binds to the IL-1 receptor type 1 (IL-1R1). Then the co-receptor chain, termed the accessory protein (IL-1RAcP), is recruited. This triple complex recruits the adaptor protein MyD88 to the Toll-IL-1 receptor (TIR) domain. Several kinases are phosphorylated, nuclear factor-κB (NF-κB) translocates to the nucleus, and pro-ILβ transcription ensues. The NLRP3-inflammasome is a cytosolic molecular structure composed of an adaptor protein, pro-caspase 1, and the NLRP3 sensor molecule, which may be activated by both infectious stimuli, known as pathogen-associated molecular patterns (PAMPs) and sterile stimuli, known as damage-associated molecular patterns (DAMPs). This activation is based on either ATP binding to the P2X7 receptor with a secondary efflux of potassium to the extracellular space or reactive oxygen species (ROS) formation. Upon activation of the NLRP3-inflammasome, pro-caspase-1 is converted to an active enzyme. Active caspase-1 then cleaves the IL-1 precursor in specialized secretory lysosomes or in the cytosol, followed by secretion of “mature” IL-1β.

That paper refers to experimental demonstration of Heart Damage by Endotoxin induction of IL-1β in Mice.¹³

Endotoxin Induced Myocarditis is routinely used in animal models to test the effects of drugs.¹⁴

Eosinophilic Myocarditis from Endotoxin

Various stains are used to investigate cells involved in Myocarditis, and particular stains for Eosinophilic cells as indication of phagocytosis have been used in Endotoxin Myocarditis.¹⁵

Heart Damage should vary by Jab Lot or Batch

Endotoxin is a major factor in Heart Damage caused by Pfizer jabs, so we should see more damage with more Endotoxin. We must press for urgent release of all assays.

1. Production of the Pfizer BioNTech mRNA jabs

2. Barbara Gehrett, MD; Joseph Gehrett, MD; Chris Flowers, MD; and Loree Britt. 19 January 2023. 77% of Cardiovascular Adverse Events from Pfizer’s mRNA COVID Shot Occurred in Women, as Well as in People Under Age 65. Two Minors Suffered Cardiac Events. https://dailyclout.io/report-53-cardiovascular-adverse-events/

3. Stephanie Seneff, Greg Nigh, Anthony M Kyriakopoulus and Peter A McCullough. June 2022.Innate immune suppression by SARS-CoV-2 mRNA vaccinations: The role of G-quadruplexes, exosomes, and MicroRNAs. https://www.sciencedirect.com/science/article/pii/S027869152200206X

4. Xian-Ke Qiu and Jun Ma. 2018. Alteration in microRNA-155 level correspond to severity of coronary heart disease. https://www.tandfonline.com/doi/abs/10.1080/00365513.2018.1435904

5. Chungxiao Wang et al. 2017. Macrophage-Derived mir-155-Containing Exosomes Suppress Fibroblast Proliferation and Promote Fibroblast Inflammation during Cardiac Injury. https://www.sciencedirect.com/science/article/pii/S1525001616453645

6. Esmerina Tili et al. 2007. Modulation of miR-155 and miR-125b Levels following Lipopolysaccharide/TNF-α Stimulation and Their Possible Roles in Regulating the Response to Endotoxin Shock https://journals.aai.org/jimmunol/article/179/8/5082/111528/Modulation-of-miR-155-and-miR-125b-Levels

7. AbdelMassih A, et al. 2022. The role of miRNAs in viral myocarditis, and its possible implication in induction of mRNA-based COVID-19 vaccines-induced myocarditis. https://bnrc.springeropen.com/articles/10.1186/s42269-022-00955-1

8. Zhang Y, et al. 2016. Silencing MicroRNA-155 Attenuates Cardiac Injury and Dysfunction in Viral Myocarditis via Promotion of M2 Phenotype Polarization of Macrophages. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773853/

9. Vasques-Nóvoa F, et al. 2018. MicroRNA-155 Amplifies Nitric Oxide/cGMP Signaling and Impairs Vascular Angiotensin II Reactivity in Septic Shock. https://journals.lww.com/ccmjournal/abstract/2018/09000/microrna_155_amplifies_nitric_oxide_cgmp_signaling.39.aspx

10. Schürch CM, et al. 2018. The “don't eat me” signal CD47 is a novel diagnostic biomarker and potential therapeutic target for diffuse malignant mesothelioma. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739575/

11. Ong J, et al. 2019. Age-related gene and miRNA expression changes in airways of healthy individuals. https://www.nature.com/articles/s41598-019-39873-0

12. Szekely Y, et al. 2018. A Review of Interleukin-1 in Heart Disease: Where Do We Stand Today? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986669/

13. De Jesus NM, et al. 2015. Atherosclerosis exacerbates arrhythmia following myocardial infarction: Role of myocardial inflammation. https://www.heartrhythmjournal.com/article/S1547-5271(14)01134-5/fulltext

14. Li F, et al. 2017. Apigenin Alleviates Endotoxin-Induced Myocardial Toxicity by Modulating Inflammation, Oxidative Stress, and Autophagy. https://www.hindawi.com/journals/omcl/2017/2302896/

15. Wong M-L, et al. 2003. Identification, characterization, and gene expression profiling of endotoxin-induced myocarditis. https://www.pnas.org/doi/full/10.1073/pnas.2336220100