Lipid Nanoparticle-Associated Inflammation is Triggered by Galectin Activation Which Are Involved In Cancer Propagation


A new preprint paper was published showing that the Lipid Nanoparticles used as a delivery platform of the C19 bioweapons cause massive inflammation and aggravate preexisting inflammation. Inflammation accelerates aging and hence causes all diseases of aging, including cancer. This damning report shows that the endosomal escape which is how the modRNA works, also causes inflammation and damage.

Inhibition of Galectins can help reverse this inflammation. While scientists are still arguing about the C19 bioweapon toxicity and the correlation to accelerated aging blood clotting and turbo cancers, I have long shown that the lipid nanoparticle self assembly is a major extinction level event in human blood. Understanding Galectin pathways could be an important way to help the C19 injected, preventatively and therapeutically – and could be considered as a preventative measure for shedding as well. I am not referring to clearing the blood, but to downregulate the inflammatory cascade that increases the risk for cancer as well.

Lipid Nanoparticle-Associated Inflammation is Triggered by Sensing of Endosomal Damage: Engineering Endosomal Escape Without Side Effects

Lipid nanoparticles (LNPs) have emerged as the dominant platform for RNA delivery, based on their success in the COVID-19 vaccines and late-stage clinical studies in other indications. However, we and others have shown that LNPs induce severe inflammation, and massively aggravate pre-existing inflammation. Here, using structure-function screening of lipids and analyses of signaling pathways, we elucidate the mechanisms of LNP-associated inflammation and demonstrate solutions. We show that LNPs’ hallmark feature, endosomal escape, which is necessary for RNA expression, also directly triggers inflammation by causing endosomal membrane damage. Large, irreparable, endosomal holes are recognized by cytosolic proteins called galectins, which bind to sugars on the inner endosomal membrane and then regulate downstream inflammation. We find that inhibition of galectins abrogates LNP-associated inflammation, both in vitro and in vivo . We show that rapidly biodegradable ionizable lipids can preferentially create endosomal holes that are smaller in size and reparable by the endosomal sorting complex required for transport (ESCRT) pathway. Ionizable lipids producing such ESCRT-recruiting endosomal holes can produce high expression from cargo mRNA with minimal inflammation. Finally, we show that both routes to non-inflammatory LNPs, either galectin inhibition or ESCRT-recruiting ionizable lipids, are compatible with therapeutic mRNAs that ameliorate inflammation in disease models. LNPs without galectin inhibition or biodegradable ionizable lipids lead to severe exacerbation of inflammation in these models. In summary, endosomal escape induces endosomal membrane damage that can lead to inflammation. However, the inflammation can be controlled by inhibiting galectins (large hole detectors) or by using biodegradable lipids, which create smaller holes that are reparable by the ESCRT pathway. These strategies should lead to generally safer LNPs that can be used to treat inflammatory diseases.

What do Galectins do? They are involved in cell signalling and cancer development:


Galectins are glycan-binding proteins implicated in intracellular signaling, cell–cell communication, cellular proliferation and survival. These endogenous lectins have emerged as key players in the tumor microenvironment. They are expressed and released by different cell types, including tumor, stromal, endothelial and immune cells. Galectins critically influence tumor progression by modulating tumor cell migration, invasiveness, angiogenesis and antitumor immune responses. Intracellularly, galectins modulate survival and proliferation and they interact with a variety of signaling pathways. Given these extracellular and intracellular functions and their regulated expression at sites of tumor growth and metastasis, galectins have stimulated great interest as relevant biomarkers and novel targets in cancer therapy.

Is it any wonder that the C19 bioweapons have caused an explosion of turbo cancers? It the lipid nanoparticle which is the platform of these injections and gene modifying technologies causing the rise in cancer via galectin activation?

This was recently discussed by the UK Expose, citing Dr McCulloughs theory of spike proteins causing the increase in cancer rates.

All mRNA injections, including cancer vaccines, may accelerate the development of cancer

I would like to suggest that this inflammatory cascade could be working via the Lipid Nanoparticles as discussed in the above cited preprint article.

Galectin inhibition has been used in cancer treatments:

Targeting galectin-driven regulatory circuits in cancer and fibrosis

Galectins are a family of endogenous glycan-binding proteins that have crucial roles in a broad range of physiological and pathological processes. As a group, these proteins use both extracellular and intracellular mechanisms as well as glycan-dependent and independent pathways to reprogramme the fate and function of numerous cell types.

What natural molecules inhibit cancer causing Galectin pathways, have profound anti inflammatory properties and could help the C19 injected as well as those affected by shedding, hence everybody in the world while avoiding poisenous Big Pharma drugs?


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