A Cellular Peine Forte et Dure: The Spike Protein Induces Almost Imperceptible Chronic Inflammation with Devastating Consequences

The key cytokine is almost certainly CCL2, and this was known in 2010!

The elevation of CCL2 expression in SARS-CoV VLP-treated and SARS-CoV spike protein-treated A549 and Vero E6 cells. RNA was isolated from A549 cells at 24 h (A) or at indicated time points (B) after the treatment of purified SARS-CoV VLPs or SARS-CoV(EM) VLPs at a VLP-to-cell ratio of 10:1 or of the viral spike protein (1 μg/106 cells) as indicated. The level of CCL2 mRNA was determined by quantitative real-time PCR. In panel A, the CCL2 mRNA in Vero E6 cells was analyzed as a comparison. In addition, culture medium of the A549 cells was collected at 24 h after the treatment and subjected to ELISA to determine the level of secreted CCL2 (C). Cells without any of the treatments were analyzed in parallel as the controls. The results shown represent the means plus standard deviations (error bars) from four independent experiments. ***, P < 0.001; **, P < 0.01 (for comparisons between the treated and untreated control cells).

The image above, which you are viewing, is NOT from cutting edge SARS-CoV-2 research. It is from a study done well over a decade ago, in 2010, on SARS-CoV. What the authors discovered is that the Spike Protein itself was able to induce upregulation of CCL2.

To understand the pathogenesis of SARS-CoV, human type II pneumocyte (A549) cells were incubated with the viral spike protein or with SARS-CoV virus-like particles containing the viral spike protein to examine cytokine modulation in lung cells. Results from oligonucleotide-based microarray, real-time PCR, and enzyme-linked immunosorbent assays indicated an upregulation of the fibrosis-associated chemokine (C-C motif) ligand 2 (CCL2) by the viral spike protein and the virus-like particles.

Upregulation of the Chemokine (C-C Motif) Ligand 2 via a Severe Acute Respiratory Syndrome Coronavirus Spike-ACE2 Signaling Pathway
https://journals.asm.org/doi/10.1128/jvi.02560-09

Why is upregulation of CCL2 (MCP-1) important and why is it dangerous?

CCL2 is expressed in, among other cells, endothelial cells. It is at Ground Zero of what I have called Spike Protein Endothelial Disease (SPED). I believe this to be an initial condition (invasion) that leads to global organ dysfunction and destruction. Please search my Substack for background. CCL2 is involved in much SARS-CoV-2 sequelae.

CCL2 is produced by many cell types, including endothelial, fibroblasts, epithelial, smooth muscle, mesangial, astrocytic, monocytic, and microglial cells (Cushing and others 1990; Standiford and others 1991; Brown and others 1992; Barna and others 1994). These cells are important for antiviral immune responses in the peripheral circulation and in tissues. However, monocyte/macrophages are found to be the major source of CCL2 (Yoshimura and others 1989a,b). CCL2 regulates the migration and infiltration of monocytes, memory T lymphocytes, and natural killer (NK) cells. Note that CCL2 is among the most studied member of the chemokine family, and has been shown to be a potential intervention point for the treatment of various diseases, including multiple sclerosis (Sorensen and others 2004), rheumatoid arthritis (Hayashida and others 2001), atherosclerosis (Kusano and others 2004), and insulin-resistant diabetes (Sartipy and others 2003).

Monocyte Chemoattractant Protein-1 (MCP-1): An Overview
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755091/

It is also responsible, most critically, for FIBROSIS.

Among chemokines, CCL2 has been identified as the most critical chemokine for tissue fibrosis and inflammation in systemic sclerosis (SSc). In patients with SSc, CCL2 levels are increased in serum, along with enhanced CCL2 expression in the epidermis, inflammatory mononuclear cells, and endothelial cells.

Chemokines in tissue fibrosis
https://www.sciencedirect.com/science/article/pii/S0925443912002554

Just as I have previously hypothesized that the Spike Protein is inducing almost imperceptible “micro-tumors,” I have also hypothesized about it causing constant organ damage. This is through inducing almost imperceptible constant inflammation, which, ultimately also explains the accelerated aging I predicted the virus and its Spike Protein would cause. There is now proof of this mechanism.

A study published Friday proves that this low-level, constant inflammation is, indeed, occurring.

Globally, over 65 million individuals are estimated to suffer from post-acute sequelae of COVID-19 (PASC). A large number of individuals living with PASC experience cardiovascular symptoms (i.e. chest pain and heart palpitations) (PASC-CVS). The role of chronic inflammation in these symptoms, in particular in individuals with symptoms persisting for >1 year after SARS-CoV-2 infection, remains to be clearly defined. In this cross-sectional study, blood samples were obtained from three different sites in Australia from individuals with i) a resolved SARS-CoV-2 infection (and no persistent symptoms i.e. Recovered), ii) individuals with prolonged PASC-CVS and iii) SARS-CoV-2 negative individuals. Individuals with PASC-CVS, relative to Recovered individuals, had a blood transcriptomic signature associated with inflammation. This was accompanied by elevated levels of pro-inflammatory cytokines (IL-12, IL-1beta;, MCP-1 and IL-6) at approximately 18 months post-infection. These cytokines were present in trace amounts, such that they could only be detected with the use of novel nanotechnology. Importantly, these trace-level cytokines had a direct effect on the functionality of pluripotent stem cell derived cardiomyocytes in vitro.

Cardiovascular symptoms of PASC are associated with trace-level cytokines that affect the function of human pluripotent stem cell derived cardiomyocytes
https://www.biorxiv.org/content/10.1101/2024.04.11.587623v1

This slow burn. Eroding all organs little by little. It is Bond-level diabolical. Of course, certain authorities would have us believe that the Bat and the Pangolin have managed to “create” one of the most stealthy and cruel conditions one could conceive – imagine what Humans could do!

We must investigate further. I believe that  the Spike, via its amyloidogenic properties, either self-replicates, or is retrotranscribed into host DNA, or both. This is also further evidence that avoiding the Spike Protein (in ALL of its forms) and keeping an anti-inflammatory diet is critical. At least until we have a full understanding of the long-term effects of the Spike Protein and how to deal with them.

Thank you, as always, for your support, readership and dialog.