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Aloë Vera & the immune system.

Aloë Vera & the immune system.

I translated this by hand because there's no good texts on Aloë Vera. (I understand like 30% of this text only).

disclaimer: (this text isn't saying you should or shouldn't take it either, nor am I, it could be horrible for crohn because of the cytokine release, or maybe it's good because it's helping to kill macrophages, I dunno. I only know some people are taking it without really knowing what it does. Aloë vera is not that innocent as I see it presented in commercials, in some way it has an effect on the immune system. This text is based on dermal use for burn wounds, as are almost all texts of Aloë vera, I can't find a single good text about crohn and Aloë vera, this is the closest I can find, this text has nothing to do with crohn)

(acemannan is the substance in Aloë Vera that affects the immune system, NO is nitric oxide released by macrophages)

Thanks to the person who made this text, <3.


Aloe Vera & the immune system.

As written in the introduction, acemannan are atm most important for dermal use. Research has shown that acemannan has some effect on macrophages, dentric cells and T-cells. In this chapter, all currently known effects of acemanan will be discussed.

4.1 Effect of acemannan on macrophages

Acemannan have diverse effects on macrophages. They make macrophages release diverse cytokine and NO. Besides that, acemannan takes care of apoptosis of macrophages. It has been shown that acemannan can increase (upregulate) the expression of diverse membrane protein. Below is detailed what the effects are of acemannan on macrophages.

4.1.1 Delivery of nitric oxide

Acemannan provide release of nitric oxide (NO). No is produced by iNOS. If macrophages are only stimulated by acemannen, they don't seem to produce iNOS from RNA, but they do in combination with IFN-y. (fig 16, lines 7-11)

Conversely, IFN-y can only lead to the production of mRNA of iNOS (fig 15, lines 1-6), if the concentration is higher than 10 units/ml. In combination with acemannan, there seems to be a synergetyc effect, the concentration of mRNA iNOS seem to be higher (bands are thicker). When 50 µg/ml acemannan are added to lines 1-5 of fig. 15, we get linkes 6-10. Now it seems that the production of mRNA iNOS is already starting at 1 unit / ml IFN-y. Besides that, when there is critically looked at Line 9 of fig. 16 and line 7 of figure 15, these two bands should have the same intensity, because the concentration of acemannan (= 50 µg/ml) and IFN-y (= 1 unit/ml) are the same. Eyeballing, the 2 bands aren't the same, Line 7 of fig. 15 seems to be a bit more pronounced. Looking at the controle (G3PD)-bands, they seem to be also more intestine with figure 15. Measuring B is maybe measured differently, this could be a possible explanation.

From the abose results there is also an increase of NOS-proteins. These proteins produce more NO (figure 17). The advantage of a higher concentration of NO is that NO has an antipathogenic working and vasodilitation, whereby more lymphocytes can go to the place of infection so they can help mediate the infection.

4.1.2 Release of cytokine.

Acemannan make diverse cytokine release from macrophages. Under influence of acemannan, interleukin-6 (IL-6) and tumor necrosis alpha (TNF-alpha) is released.
In contradiction to the NO production, is with IL-6 and TNF-alpha no IFN-y necessary (figure 18 and fiture 19). But when IFN-y is added, the concentration of IL-6 and TNF-alpha increase by about 40%.

4.1.3 Expression of adhesion moleculs and receptors

Adhesion molecules normally don't come to expression on the membrane of a macrophage who is in rest. After the macrophages are treated with a combination of acemanannen and IFN-y, the CD11a receptor did come to expression. Besides, only acemannen of IFN-y don't express CD11a. Acemannen and IFN-y make sure the expression of adhesion molecule CD18 is increased. CD18 normally does express macrophages in rest.
Mac-1 adhesion molecule is not influenced by IFN-y, acemannan is a combination of that.
Acemannan are only responsible for the expression of Fc-gamma (Fc-y) receptor of macrophages.
The CD32 and CD16 components.
Possibly increased expression of these adhesion molecules means that there's increased cell activity of macrophages and the macrophages has increased fogacyting workings. Besides that, I assume that the macrophages will be quicker to the place of infection, because the expression of CD18 is increased.
Since ICAM-1 subrstared is for the MAC-1 integrine, and because ICAM-1 adhesion molecules will come to expression during an immune reaction, macrophages will be faster to the place of infection.

Research has shown that the expression of MHCII-receptor is significant (p<= o,o5) increased, after addition of acemannan. this effect was still present after 3 days. The advantage of this increase is that TH-cells with a CD4+-receptor give off IL-2, whereby there is more proliferation of T and B-cells and the pathogen can be cleaned up faster.

4.1.4 Induction of apoptosis

As described above, acemannan has an influence on macrophages. Besides the increased expression of NO, acemannan also induce induction of apoptosis of macrophages. Apoptosis is programmed cell death. the advantage of apoptosis of macrophages is that bacteria and viruses who are fagocytosed, will die sooner. The disadvantage is that unripe and empty macrophages will die when the NO concentration is too high.

The explanation of why acemannan and IFN-y induce apoptosis of a macrophage is because acemannan and IFN-y slow down the bcl-2protein 12 to 24 after administration. The bcl-2 protein is an anit-apoptose protein. It makes sure that cells (here macrophages) don't die. Besided bcl-2 there are other proteins, who prevent apoptosis. It isn't known if acemannan stops those other proteins.

4.2 Effect of acemannan on dentric cells

Besides the influence on macrophages, acemannan also influences dnetric cells. They induce cytokine and increase certain receptors.

4.3 Release of cytokine

Acemannan induce and stimulate release of IL-12 from dentric cells. Tested with 100 µg/ml acemannan provide a blan test. IL-12 (in combination with IL-4) is important in riping of T-cells.

4.2.2 Expresison of adhesion molecules and receptors.

Research has shown that acemannan stimulate the development of dentric cells. Dentric cells exposed to acemannan riped faster than controls at 100 µg/ml concentration. The result of the faster riping was that the MHC-II receptors increased then when given a lower concentration (10µg/ml).
Besides the MHC-II recepter, the expression of CD80, CD86, CD40 and CD54 increased.

4.3 Effect on acemannan and T-cells

There isn't much research done on the influence of acemannan on T-cell. There is just on research done with acemannan on an alloantigenic reaction of mixed leukotine culture (humans and rats).

Acemannan seem to increase the T-cel activity with about 60%.

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The effects of aloe ingestion on Crohn's seems vague. Maybe others can do more research, but specific polysaccharide ranges, with a molecular weight between 5 and 400 KDa, seem to have all the immunomodulating effects--whether these effects balance or over-activate the innate immune system is not clear to me.

The claims made on the aloe's therapeutic effects range from the antioxidant effect of scavenging free radicals better than Vit E; the activation of endogenous antioxidant enzyme systems (glutathione/SOD/catalase); the boosted absorption of vitamins E (269%) and C (204%) in human plasma levels--sustained over 24 hrs--when ingested together; activation of Phase II metabolism and detoxification of pollutants via boosting liver antioxidant enzymes; and immunomodulating effects of specific polysaccharides (molecular weight range:between 5 and 400 KDa) that stimulate TNF-α (a cytokine that activates the immune system) in cultured mouse peritoneal macrophages (The peritoneal cavity is a membrane-bound and fluid-filled abdominal cavity of mammals, which contains the liver, spleen, most of the gastro-intestinal tract and other viscera. It harbors a number of immune cells including macrophages, B cells and T cells.) implanted with sarcoma cells.

More specific aloe studies dealing with in vivo mice cells implanted with sarcoma tumors:
Qui Z, et al. Modified Aloe barbadensis polysaccharide with immunoregulatory activity. Planta Medica. 2000;66:1-5.

Im S-A, et al. Identification of optimal molecular size of modified Aloe polysaccharides with maximum immunomodulatory activity. Int Immunopharmacol. 2005;5:271-279.

"Safety studies conducted on a proprietary high-purity aloe vera inner leaf fillet preparation, Qmatrix®"

This concerns a particular patented formula called ACTIValoe which is organic inner fillet and filtered leaf combined with L. Rhamnosus lysate and L-Leucine. The safety study link refers to a 90 day study--longer than any GMO study--which fed mice the stuff up to 2 grams per 2lbs body weight. If I'm reading this right, it seems they gave the mice super doses just to prove a point, I mean, the human dose is not even 1.5 grams.

The gubamint, for some reason, felt it necessary to do a study on a specific non-decolored whole leaf liquid here:

*It seems their carcinogenic mixture was with all the latex components intact. However, their own study says that most commercial products contain less than 10ppm of such latex. See pg 23 of study. Pg 32 explains immunomodulation effects. I would encourage others to research this further. I am too lazy right now.*

They concluded, after seeing carcinogenic effects of giving mice unfiltered whole leaf extract in water everyday, "The Aloe gel, which is used in skin care products, is generally believed to be safe. So, really there are three points I'd like to make from the NTP studies. Firstly, that within these NTP studies, we found there was clear carcinogenic activity of the non-decolorized whole leaf extract, in both male and female rats, based on the increase in large intestinal tumors. Now, secondly, we believe these are relevant to humans. Thirdly, how this translates to human risk requires more information. We particularly need to know what are the constituents, what's the levels of those constituents in human products, and what's the patterns of human exposure. That allows you to translate that to human risk."