Peine dur et forte on the circulatory system: the inevitable induction of fibrosis: Spike Protein Endothelial Disease (SPED)

August 27, 2022

Back to B(asics) Cells.


One very interesting aspect of SARS-CoV-2 is that the initial Plasmablast (the B Cells that secrete antibodies) response is to secrete a lot of IgA. These antibodies are useful – and notorious. They are responsible for causing vasculitis. In particular, microvessel vasculitis.

However, this is actually Stage 2 in what I am now calling Spike Protein Endothelial Disease (SPED). It is also ironic that what neutralizes the Spike Protein, also destroys the microvasculature. The Spike Protein delivers a solid One-Two Punch to the microvasculature – and then the body heals (sometimes overheals) causing even more catastrophic damage.


It is known that the Spike Protein attacks the endothelium.

Although the use of a noninfectious pseudovirus is a limitation to this study, our data reveals that S protein alone can damage endothelium, manifested by impaired mitochondrial function and eNOS activity but increased glycolysis. It appears that S protein in ECs increases redox stress which may lead to AMPK deactivation, MDM2 upregulation, and ultimately ACE2 destabilization.

SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2

This inflammatory assault of the Spike Protein on the Endothelium leads to narrowed lumen (the “tube” that the blood flows through in blood vessels). What else does this? Obesity! The processes of obesity-induced endothelial dysfunction are characterized by vascular remodeling leading to atherosclerotic plaque and narrowing of the endothelial lumen.

But, you may ask why am I making this comparison? Because of the IDENTICAL cytokine signature of Obesity and the Spike Protein!

Accumulation of excessive macronutrients on the adipose tissues promotes the secretion and release of inflammatory mediators, including interleukin-6 (IL-6), interleukin 1β, tumor necrotic factor-α (TNF-α), leptin, and stimulation of monocyte chemoattractant protein-1 (MCP-1), which subsequently reduce the production of adiponectin thereby initiating a proinflammatory state.

Endothelial Dysfunction in Obesity-Induced Inflammation: Molecular Mechanisms and Clinical Implications

We can actually look at BNT162b2 for proof of the Spike Protein inducing THIS VERY SAME PROFILE, but, ONLY AFTER THE SECOND VACCINATION!

We identify a systemic signature including increases in IL-15, IFN-g, and IP-10/CXCL10 after the 1st vaccination, which were enriched by tumor necrosis factor alpha (TNF-a) and IL-6 after the 2nd vaccination… Importantly, TNF-a, MCP-1/CCL2, IL-7, IL-3, and IL-12/IL-23p40 showed significant increases only after the 2nd vaccination (day 23).

Systemic IL-15, IFN-g, and IP-10/CXCL10 signature associated with effective immune response to SARS-CoV-2 in BNT162b2 mRNA vaccine recipients

So, in essence, the Spike Protein gives you the systemic signature of THE OBESE. Understandably, if you are ALREADY OBESE, this could obviously be MUCH WORSE.


Now we come to my initial remark, that the antibody response to SARS-CoV-2 is initially a significant IgA response. These antibodies can form complexes (they group together) and are then deposited into the microvasculature, DAMAGING THE MICROVASCULATURE AGAIN.

IgA vasculitis, formerly Henoch-Schönlein purpura, is a form of vasculitis—a family of rare disorders characterized by inflammation of the blood vessels, which can restrict blood flow and damage vital organs and tissues. IgA (immunoglobulin A) vasculitis causes inflammation and bleeding of the small blood vessels of the skin, joints, intestines and kidneys. Rarely, it can affect the lungs and central nervous system. It is the most common form of vasculitis in children.

IgA vasculitis is systemic, meaning it can affect all organ systems in the body. The most characteristic symptom is a raised, purplish skin rash that resembles bruises, mostly affecting the legs and buttocks. Other common symptoms or signs of organ involvement include abdominal pain, joint pain and swelling, and kidney inflammation.

IgA Vasculitis

Current research suggests the role of IgA-mediated immune response, evidenced by early seroconversion to IgA in COVID-19 patients and the role of IgA in immune hyperactivation as the predominant mediator of the disease process.

The pathogenesis of COVID-19-induced IgA nephropathy and IgA vasculitis: A systematic review

With regards to our dear friend BNT162b2 we notice a disturbing finding.

Serum IgA concentration reaches a plateau after a single dose in seropositive individuals and two vaccine doses in seronegative subjects. After the second dose IgA level was higher in seronegative than in seropositive subjects. In saliva, IgG level is almost two orders of magnitude lower than in serum, reaching the highest values after the second dose. IgA concentration remains low and increases significantly only in seropositive individuals after the second dose. Neutralizing antibody titres were much higher in serum than in saliva.

Mucosal immune response in BNT162b2 COVID-19 vaccine recipients

How do we know this can be pathogenic? There are myriad examples. I offer this one.

IgA Nephropathy After SARS-CoV-2 Vaccination


Ultimately, we arrive at THE POINT. Vasculitis is a deadly serious disease. It used to be rare (like so many other diseases, until recently…). Once a blood vessel is affected by vasculitis, it is NEVER the same. It will suffer permanent damage. The healing process causes scarring. This is natural. The same process happens when you get stitches. The new tissue is tougher, less pliable, thicker, FIBROUS. Now, you have A LOT of room to play with concerning your skin. Getting some thick, tough skin on your arm ain’t gonna stop you from using your arm. When you are dealing with VERY, VERY SMALL BLOOD VESSELS, scarring can wipe them out. Obliterate them. If not in one pass, then in several.


Here’s an example.

Three patients lacked arterial wall enhancement, and these all had reversal of arterial narrowing within 3 months. Four patients demonstrated arterial wall enhancement, and these had persistent or progressive arterial narrowing at a median follow-up of 17 months (range, 6–36 months) with final diagnoses of central nervous system vasculitis and cocaine vasculopathy.

Vessel Wall MRI to Differentiate Between Reversible Cerebral Vasoconstriction Syndrome and Central Nervous System Vasculitis


And yet we are now looking at boosters – with the original Spike and the initial Omicron. Both extinct variants.

So, as with the trash compactor in Star Wars, our heroes, our microvessels that feed and oxygenate our entire body, are slow being squeezed to death.

Madness. Madness. Madness.

Referenced/Related Papers

A Review of the Mechanism of Vascular Endothelial Injury in Immunoglobulin A Vasculitis

Vasculitis Pathophysiology Overview