Transfer factors and Inflammation

Transfer factors and Inflammation
I am posting an article below that I wrote on transfer factors and inflammation. transfer factors is a "smart" molecule or regulator molecule. There are hundreds of functions within your body's immune system, antioxidant system and detox system. How does these cells and molecules know what to do and when to do it? Smart cells or molecules direct and regulate these functions.

Transfer factors influence the actions of many immune system components. There are a number of cells that can secrete chemicals that cause inflammation. For example transfer factors can signal Natural Killer Cells into increased action. NK Cells can secrete a chemical that can cause inflammation. By regulating NK Cells, transfer factors can regulate the inflammation caused by this chemical. Mike

Understanding inflammation, disease, competition 

There has been a great deal of talk about inflammation in our industry lately. A few of our competitors refer to inhibiting the cox-2 enzyme. This article is to assist you in understanding inflammation and how it operates in our bodies. Once you understand the positive purpose of inflammation and how inflammation becomes dangerous, you can then understand how regulators such as transfer factors are superior over inhibitors such as xanthones found in mangosteen.

There are many genes, enzymes, body chemicals, immune system cells and molecules involved in the inflammation pathway. I am sure many of you have read about drugs that inhibit just one of the agents such as cox-2 involved in inflammation causing heart disease. There is a great deal to learn about inflammation and how to control its effect on our health.

We all are effected inflammation both good and bad. The more we understand the more we can be in control of our health.

Controlled inflammation is a good thing and very important to our health. Inflammation is the immune system’s first reaction to an infectious invader, an injury, irritation or stressor (such as pollution, cigarette smoke, free radicals etc.). Chemical sensors detect an injury, infectious invader etc. and call for the release of the molecule nuclear factor-kappa beta (NFkB). NFkB is found in the cytoplasm of every cell and is bound to certain proteins that keep it inactive.

Once NFkB is released it travels to the nucleus and binds to the DNA. It acts as a switch turning on and off more than 400 genes. These genes command the productions of a number of various enzymes that create a cascade of events that result in inflammation.

The positive actions of inflammation are the dilation of blood vessels upstream from an infection or injury and the constriction of vessel downstream. Capillary permeability to the effected areas is increased.

The increase in the permeability of the capillaries allows the white blood cells, containing the immune system, to filter out into the effected tissue. Immune system cells and molecules such as phagocytes pick up bacteria and debris. The inflammation walls off the infected area preventing its spread.

You can see from my illustration that you want to regulate inflammation and not eliminate it completely. This is the difference between regulation and inhibition. The real problem begins when the inflammation persists. A healthy immune system will respond to a crisis and wall off an area in order for immune system components to destroy or remove the threat and allow the body to heal itself.

When the process takes too long, chronic inflammation is the result. Neutrophils are the first to appear in an infected area. These neutrophils release chemical messengers that communicate with a variety of players in the healing process. Neutrophils only live for a couple of days.

If battle or process persists, the neutrophils are replaced by longer lived immune system components such as monocytes, macrophages, T-cytotoxic, T-helper, memory T cells and B cells (which produce antibodies). The process through which these major players enter the battlefield is through the continued presence of NFkB. Cytokines (communication cells) IL-1 and TNF instruct endothelial cells to up-regulate receptors for these immune cells to enter the effected area.

The endothelial cells line the inside of your arteries and capillaries. The endothelial lining controls what is release from the blood into the tissue. I think many of you will remember that chronic inflammation of the artery lining is now believed to be a major cause of heart disease.

Also in this cascade of events histamine and protaglandins are released. Many different chemicals are produced and released during this process such as cox-2, TNF-alpha, Interleukin-6, interleukin-1 beta, interkeulin-8 and lipoxygenase which all play a role in chronic inflammation.

Inflammation begins as a immune system response to control an infection or some other threat but progresses into a chronic stage which can lead to heart disease, cancer, diabetes, arthritis, Alzheimer’s, autoimmune conditions and many other life threatening challenges.

As we age, we generally develop chronic inflammation throughout our bodies, which leads to premature aging, disease and a general fatigue condition.

There is a vicious cycle that develops within our bodies of the turning on of genes, the expression of various chemicals and activation of various immune system cells. There are a number of regulators involved in this cascade of events. Consuming one nutrient to inhibit one enzyme involved in inflammation is like throwing a pebble into a sea.

Transfer factors are master regulators that are already in our bodies. We do not know all of the functions of transfer factors as of yet. The science of understanding transfer factors is an ever-expanding arena. We do know that transfer factors regulate a number of immune system cells and chemicals that are involved in the process referred to above.

Also we know that transfer factors increase the immune system’s effectiveness. One of the reasons for chronic inflammation is the persistence of the original aggravating threat whether it is a bacteria infection or some other threat. As an example some enhanced transfer factors have been found to increase the activity of natural killer cells by 437%. The more effective the immune system response the faster the threat is eliminated and quicker inflammation is not needed.

If you are over 40 years old, it is very likely that you have the beginning stages of some kind of inflammation. I suggest that you approach this challenge from a preventative position and not from a reactive position. Once cancer, Alzheimer’s, or heart disease develops, you have a life-threatening challenge.

A product using transfer factors should be the foundation for a healthy future. Also consuming antioxidants is a must for a bright and healthy future. If you already have an inflammation problem, then add a joint supplement to your regimen. With this arsenal you are approaching inflammation from several directions.

Add exercise and as close to a balanced diet as possible to your nutritional regimen and you can enjoy the last half of your extended life.
 
Inflamm Res. 2005 Feb;54(2):74-81.
 
Dialyzable leukocyte extract differentially regulates the production of TNFalpha, IL-6, and IL-8 in bacterial component-activated leukocytes and endothelial cells.

Ojeda MO, van't Veer C, Fernández Ortega CB, Araña Rosainz Mde J, Buurman WA.
Division of Physical Chemistry, Center for Genetic Engineering and Biotechnology (CIGB), P.O. Box 6162, Havana, 10600, Cuba. miriam.ojeda@cigb.edu.cu
 
OBJECTIVE: To investigate i) whether the Dialyzable Leukocyte Extract (DLE) modulates the production of proinflammatory cytokines in leukocytes activated by the bacterial cell wall components lipopolysaccharide (LPS), lipoteichoic acid (LTA), and peptidoglycan (PGN); ii) the effect of DLE on LPS-stimulated endothelial cells; and iii) whether the regulatory effect of DLE on inflammatory mediators is related to the modulation of Toll-like receptors (TLRs), NF-kappaB and cAMP signaling pathways.
 
METHODS: Leukocytes were stimulated with LPS, LTA, and PGN in the presence of DLE. Endothelial cells were stimulated with LPS and treated with DLE. The levels of Tumor Necrosis Factor-alpha(TNFalpha), Interleukin-6 (IL-6), and IL-8 in culture supernatants were evaluated by ELISA. The expression of Toll-like receptor 2 (TLR2) and 4 (TLR4), NF-kappaB activity and cAMP levels were evaluated by flow cytometry, EMSA, and EIA, respectively. RESULTS: The addition of DLE to leukocytes stimulated with cell wall constituents suppressed the production of TNFalpha. However, DLE induced IL-8 release in monocytes and enhanced IL-6 and IL-8 production by activated monocytes and endothelial cells. Also, DLE induced TLR2 and TLR4 expression, and increased cAMP levels, whereas NF-kappaB activity was inhibited. 
 
CONCLUSIONS: The present data indicate the differential regulation by DLE of the production of TNFalpha, IL-6, and IL-8 cytokines, associated with effects on TLR2 and TLR4 expression and NF-kappaB and cAMP activities. We suggest a putative mechanism for the biological effects of DLE in activated leukocytes and endothelial cells.
 
PMID: 15750714 [PubMed - indexed for MEDLINE]

1 comment:

  1. Hi Fernando,
    I am so glad to have stumbled across your article. It provided a great deal of information I was looking for, and trying to confirm. I was formerly in 4life, and considering returning to the company. My clients would benefit greatly from their products in my opinion, and your article confirmed that for me. Thank you so much for such a well written, easy to understand article on inflammation. It was exactly what I was looking for. GB

    ReplyDelete