Eotaxin Diseases caused by Endotoxin in the Jabs
Devious jab profiteers prefer to mention Eotaxin rather than Endotoxin in their patents and publications. Can you help me mine the literature? Lingering Kisses!
Using the search function in Substack I found my friend Moriarty has a keen interest in the inflammatory and other damage caused by Eotaxin, as covered in his discussion of the effects of jabbing Children with Pfizer BNT162b Covid19 jab altering the immune response to some pathogens.1
Please let me know if you find other authors who have talked about Eotaxin.
Endotoxin upregulates Eotaxin
Intraperitoneal injection of Endotoxin upregulates Eotaxin in the Serum, Peritoneal wash, and Lungs of mice.2
Eotaxin in Human Breast Cancer
Researchers in India demonstrated that Eotaxin is involved in recruiting and polarizing Tumor Associated Macrophages towards an M2-polarized phenotype.3
On the right hans side of their Figure 9, they found Bevacizumab retarded the tumor growth.
Human Eotaxins
There are 3 Human Eotaxin Genes4 numbered 1, 2 or 3 which code for their respective Eotaxn Proteins. They are also known as
CCL11 (eotaxin-1)
CCL24 (eotaxin-2)
CCL26 (eotaxin-3)
CCL stands for C-C motif Chemokine Ligand.
CCL11 gene is associated with 1,858 Diseases.5
It has numerous synonyms Cadr_000019305 | CB1_000549014 | CC chemokine ligand 11 | C-C motif chemokine 11 | chemokine CCL11/EOTAXIN | chemokine (C-C motif) ligand 11 | CK820_G0028672 | eosinophil chemotactic protein | eotaxin | eotaxin-1 | HJG63_002330 | LOW QUALITY PROTEIN: eotaxin | PAL_GLEAN10019878 | SCYA11 | small chemokine (C-C motif) ligand 11 | small inducible cytokine A11 | small-inducible cytokine A11 | small inducible cytokine subfamily A11 | small inducible cytokine subfamily A (Cys-Cys), member 11 (eotaxin)
A 2014 review6 from researchers from the Digestive Disease Institute, Shaare Zedek Medical Center, affiliated with the Hebrew University School of Medicine, Jerusalem, Israel covers a number of important Eotaxin diseases listed in their Table:
Storage and Release from Eosinophils
In 2002 it was discovered7 that Interleukin 16 (IL-16) can direct Eosinophils to make new LTC4 and release the chemokines, RANTES, and Eotaxin.
Romantic Lingering Kisses release Eotaxin
In the fascinating world of poisoning by release of Chemokines, I found a lovely paper describing the “Lingering Kiss” whereby cells release Eotaxin and other small molecules.8
Endothelial cell adhesion molecules are stored in specific intracellular compartments named Weibel Palade bodies (WPBs) along with von Willebrand factor (vWF), P-selectin, Eotaxin-3, Interleukin-8 (IL-8) and more. Endotoxin exposure mobilizes these molecules to the cell surface.
Eotaxin role in numerous tissues
Eotaxin stimulates directional migration, adhesion, accumulation, and recruitment of T lymphocytes in association with the Th1-derived cytokine IL-2 and the Th2-derived cytokine IL-4.9
Eotaxin in response to Mustard Gas
Researchers in Iran found that Eotaxin is upregulated in the lungs of people exposed to Mustard Gas.10
Jabber Interest in exposing you to Eotaxin
I briefly covered jab developers who measure Eotaxin here:
Eotaxin is involved in Pericarditis.
Eotaxin and Eye Diseases
In 2000, researchers in Japan11 investigated Eotaxin expression in response to TNF-α in synergy with Th-2 type cytokines Interleukin-4 or Interleukin-13. IL-4 induces immunoglobulin isotype switching in B cells and maintains the production of IgE. IL-13 also induces IgE production and modifies IgE-mediated allergic responses.
Eotaxin in Allergic Rhinitis
Researchers on Japan investigated Interleukin 33 (IL-33) and found cross-linkage of FcεRI on bone marrow–derived Connective Tissue–type Mast Cells (CTMCs) and Mucosal Mast Cells (MMCs) in the presence of IL-3 markedly induced production of IL-1β and Eotaxin.
IL-4 or IL-13 induced production of Eotaxin from fibroblasts is mediated by STAT6.
Question
Who thinks it is a good idea to boost Eotaxin by jabbing with Endotoxin?
Will add more references later.
Sara S. Cheng, Nicholas W. Lukacs, and Steven L. Kunkel. 2002. Eotaxin/CCL11 Is a Negative Regulator of Neutrophil Recruitment in a Murine Model of Endotoxemia. Experimental and Molecular Pathology 73: 1–8.
Chakrapani Tripathi Brij Nath Tewari, Ranjana Kumari Kanchan, Khemraj Singh Baghel, Naveen Nautiyal, Richa Shrivastava, Harbeer Kaur, Madan Lal Bramha Bhatt and Smrati Bhadauria. 2014. Macrophages are recruited to hypoxic tumor areas and acquire a Pro-Angiogenic M2-Polarized phenotype via hypoxic cancer cell derived cytokines Oncostatin M and Eotaxin. https://www.oncotarget.com/article/2110/text/
https://en.wikipedia.org/wiki/Eotaxin
https://ctdbase.org/detail.go?acc=6356&view=disease&sort=diseaseNmSort&type=gene&dir=asc
Tomer Adar, Shimon Shteingart, Ami Ben Ya'acov, Ariella Bar-Gil Shitrit, Eran Goldin. 2014. From airway inflammation to inflammatory bowel disease: Eotaxin-1, a key regulator of intestinal inflammation. Clinical Immunology 153, 199–208
Christianne Bandeira-Melo, Kumiya Sugiyama, Lesley J. Woods, Mojabeng Phoofolo, David M. Center, William W. Cruikshank, and Peter F. Weller. 2022. IL-16 Promotes Leukotriene C4 and IL-4 Release from Human Eosinophils via CD4- and Autocrine CCR3-Chemokine-Mediated Signaling. J Immunol (2002) 168 (9): 4756–4763.
Victor Babich, Athinoula Meli, Laura Knipe, John E. Dempster, Paul Skehel, Matthew J. Hannah, and Tom Carter. 2008. Selective release of molecules fromWeibel-Palade bodies during a lingering kiss. https://ashpublications.org/blood/article/111/11/5282/23318/Selective-release-of-molecules-from-Weibel-Palade
T Jinquan, S Quan, G Feili, C G Larsen, K Thestrup-Pedersen. 1999. Eotaxin activates T cells to chemotaxis and adhesion only if induced to express CCR3 by IL-2 together with IL-4. https://journals.aai.org/jimmunol/article/162/7/4285/44481/Eotaxin-Activates-T-Cells-to-Chemotaxis-and
Ali Emad and Yasaman Emad. 2007. Relationship Between Eosinophilia and Levels of Chemokines (CCL5 and CCL11) and IL-5 in Bronchoalveolar Lavage Fluid of Patients With Mustard Gas-Induced Pulmonary Fibrosis. J Clin Immunol. 27:605–612.
Naoki Kumagai, Ken Fukuda, Yoshitsugu Ishimura, and Teruo Nishida. 2000. Synergistic Induction of Eotaxin Expression in Human Keratocytes by TNF-α and IL-4 or IL-13. Invest Ophthalmol Vis Sci. 2000;41:1448–1453