Macrophages and T-Lymphocytes Secrete Collagen

There are several potential sources of origin for the capsule collagen that surrounds a dormant or benign tumor that is not a pseudo-capsule generated from compression of the stromal tissues.  One overlooked source of the capsule demonstrated by Vaage in 1991 is the immune system itself, with lymphocytes and macrophages surrounding aberrant, immunogenic cells with a collagen capsule.  Research regarding the involvement of macrophages and lymphocytes in useful and pathological collagenous fibrosis is an important facet of fibrosis mechanisms that is still highly relevant today, in 2012.  Of course, any collagen synthesis requires Vitamin C/ascorbic acid/ascorbate.  Innate defense and cytotoxic immune cells in particular use vastly large quantities of it, accumulating it against an osmotic gradient to 100-fold more than the surrounding serum or plasma.

Collagen production by macrophages in tumour encapsulation and dormancy.

Fibrous Capsule of a dormant (not growing) tumor (Vaage 1991)

T-Lymphocyte Secreted Collagen Fibers, Vaage 1991

 

 

"Millions of Cracks" in Artery Wall = Leaky Junctions

In Tarbell's research, 90% of LDL, the delivery particle that solubilizes otherwise insoluble cholesterol gets through the first layer of an artery through a "leaky junction."  The normal pores in the first layer of an artery are just too small for anything other than albumin and micromolecules in water to get through.  Nothing gets through a tight junction.  Large gaps, leaky junctions, occur only when the layer of cells divides or is injured, pulling away from each other and revealing the subintimal layer.  Only 10% of LDL gets through by active vesicular consumption. 

Stretch and Shear Interactions Affect Intercellular Junction Protein Expression and Turnover in Endothelial Cells.

Shear stress and the endothelial transport barrier

"Million of Cracks in Artery Wall" = Leaky Junction

Headline: "Deficient Cholesterol: A Common New Factor in Autism"

The importance of cholesterol to the central nervous system cannot be underestimated, as is demonstrated by this group with the improvement of symptoms with parenteral supplementation in patients:

http://www.greatplainslaboratory.com/home/eng/cholesterol.asp

Their PDF File

Hydraulic stress in thrust fittings and accelerating curves of arterial system generate inflammatory gene expression

Normal mice just don't get atherosclerosis.  Just never.  In every lab on Planet Earth, these hardy beasts must be genetically handicapped in ways that humans never are, and then poisoned with massive doses of lard or high blood pressure hormone to induce a similar pathology to that which develops in humans over decades (not overnight).  When the LDL cholesterol receptor is ablated, and then these mice insulted with the lard or AngII, they exhibit a pattern of inflammation in their arteries at the high pressure regions, the branches or "thrust fitting" joints as a master plumber would call them or in high acceleration curves.  At these points, white blood cells stick to the intimal surface, forming the first lesions of atherosclerosis called foam cell lesions that look like butter from afar, but under the microscope are distinctly living white blood cells.  As things progress further, these cells may die leaving a trash dump of necrotic debris including the accumulated cholesterol delivered via lipoproteins.

The NF-κB signal transduction pathway in aortic endothelial cells is primed for activation in regions predisposed to atherosclerotic lesion formation

The lesions don't happen haphazardly and randomly, but predictably in mechanical stress sites where inflammatory gene expression is activated, consequently drawing the ire of our own immune system cells and acute phase reactants.

The first barrier to the living wall of muscle cells of the artery are the endothelial cells that sit happily on top of their collagen basement membrane, in tight formation with not much that can slip through their cell junctions bigger than small organic molecules.  When there is damage, either directly to an endothelial cell, causing endothelial denudation, or by well meaning white blood cells causing collateral damage, the collagen membrane floor is revealed, which is sticky to many problematic things including the infamous Lp(a) which sticks to exposed lysyl residues of collagen strands.  The wall is then vulnerable to insudation by clotting systems as they should or activated platelets that stick to collagen.

To prevent all this from occurring, the thing to do would be to dial down the inflammatory signals that turn on NF-Kappa Beta, a ubiquitous nexus and hub for many inflammatory processes both useful and malignant.

As you might have guessed, there are nutritional means to do this without relying on hazardous, poisonous, expensive, and annoying prescription drugs, none of which are designated as specific NF-kappa B inhibitors anyways.

For example,
Antioxidants like Vitamin C can turn this switch off
Molecules from herb extracts can turn this switch off.
simple amino acids can halt this stress signal.
Resveratrol can turn this switch off.

and many other functional foods...