Green Tea Compound, Hypermethylation and Tregs In Allergy and Chemical Sensitivity!

Recent studies propose that environmental illnesses are caused from "loss of tolerance" and that alterations in T regulatory cells (Tregs) may be a important factor. A number of studies demonstrate health benefits from epigallocatechin gallate (EGCG) which is a compound found in green tea. Yun shows EGCG can enhance Tregs production and enhance expression of histone deacetylases while decreasing expression of NF-kappaB. It also has been shown to reactivate genes that have been silenced by hypermethylation and prevent these changes to subsequent passage to daughter cells by DNA methyltransferases. (Fang) Interestingly, CCL18 is a chemokine that is elevated in allergic patients and may contribute to the "loss of tolerance" because in normal patients it promotes the generation of normal normal Tregs but in allergic patients it does not and may
an increased prevalence for symptoms that are common with chemical sensitivity in allergic patients. In addition, other factors including the proper expression of the Nrf2 system and other pathways for antioxidant expression may mitigate the effects while impairments may exacerbate them. EGCG has been shown to act through Nrf2, although this may not be its only mode of action. In any event, EGCG may provide some therapeutic effects for these kinds of conditions.


Yun, J.-M. and Jialal, I. Effects of epigallocatechin gallate on regulatory t cell number and function in obese versus lean volunteers. FASEB.http://www.citeulike.org/user/HEIRS/article/7651808
Fang, M. Z. Z., Wang, Y., Ai, N., Hou, Z., Sun, Y., Lu, H., Welsh, W., and Yang, C. S. (2003). Tea polyphenol (-)-epigallocatechin-3-gallate inhibits dna methyltransferase and reactivates methylation-silenced genes in cancer cell lines. Cancer research, 63(22):7563-7570.
http://www.citeulike.org/user/HEIRS/article/3326104
Chang, Y., de Nadai, P., Azzaoui, I., Morales, O., Delhem, N., Vorng, H., Tomavo, S., Ait Yahia, S., Zhang, G., Wallaert, B., Chenivesse, C., and Tsicopoulos, A. (2010). The chemokine ccl18 generates adaptive regulatory t cells from memory cd4+ t cells of healthy but not allergic subjects. The FASEB journal. http://www.citeulike.org/user/HEIRS/article/7651843

Chemical Sensivity and Asthma -- Systems Theory and The Idea of Loss of Tolerance in Different Tissues!

In the last few years, environmental illness researchers have suggested that chemical sensitivity is related to a general loss of tolerance that may occur after an event such as bacterial or viral event. Of course, this would make sense given that an inflammatory event may lead to loss of tolerance through alterations in immune function and some experts believe a similar process is responsible for autoimmune-type reactions and a loss of T regulatory cells (Tregs). In general, Treg serve as a type of mediator for inflammatory conditions and modulates the type and severity of the immune reaction. In MCS, there is a loss of tolerance to chemicals in the environment at levels that normally do not effect a healthy individual. Interestingly, a recent study of asthma has shown that hypersensitivity airway responsiveness can be improved by boosting immunity in the gut. The fact that airway responsiveness can be improved through gut improvement helps to support the possibility that MCS immune dysfunction may begin in the intestinal tract or the lungs even though symptoms may not necessarily be respiratory or gut related. It has been known for two decades, the intestinal tract is an important regulator of immune and brain function but admittedly, little is known about the pathways or the process involved that makes the connections of the intestinal tract, the brain and the CNS. However, studies published last year identified inflammatory brain processes that effect gene regulation and neurotransmission can be the result of the activities of inflammatory mediators or cytokines in the gut and the liver.

Individuals with MCS often present with abnormal respiratory function and many that suffer from MCS propose they are more sensitive to carbon monoxide and hydrogen sulfide than others. I would suggest through observation this is also true of nitrous oxide and possibly other greenhouse gases and note here there have been reports of mood and behavior changes from exposures to higher levels of these gases. These reports are similar to many with MCS when they describe their reported reactive symptoms. Therefore these reactions could be the result from elevations in greenhouse gases in addition to other pollutants that combine to form explained additional "triggers".   Previously, I have suggested the loss of Nrf2 and its associated proteins such as HO-1 that regulate the gasotransmitters may be to blame and could lead to loss of tolerance or heightened reaction even to lower levels of "perceived" pollutants or chemicals in the environment.  Considering the levels of greenhouse gases are steadily increasing on the average in the environment with each decade-- the constant exposure to one may be reducing the tolerance to the cumulative total of the others or "potentiating" the effects. This brings to light an important health and policy concern since the "jury" is still out on how to reduce greenhouse gases with our present dependance on fossil fuels. Interestingly, you never really hear about the increases in greenhouse gases in relation to the causes and implications of MCS, even though it should be considered...

In any case, there is recent evidence the proteins that make up the xenobiotic detoxification system such as the Nrf2, AhR, and HO-1 may influence Treg regulation. For this reason, the effects of Treg deficiency and dysfunction should be considered why addressing the possible causes for increased sensitivities that are observed in those effected with environmental illness and why boosting gut immunity of systemic immunity may influence more than one organ system. In addition, it has been demonstrated that endotoxin a component of bacteria may lead to a heightened response from allergans. It could be endotoxic exposure leads to a heightened response to chemicals or contaminants whether endogenous or not and alterations in methylation from endotoxin may augment conditions of the "loss of tolerance" that that lead to and occur with environmental illness. Unfortunately, this "loss of tolerance" may also be the consequence of pathogens and contaminants that normally reside at low levels in different tissue and are present in the environment.




Strickland, D. H., Judd, S., Thomas, J. A., Larcombe, A. N., Sly, P. D., and Holt, P. G. (2010). Boosting airway t-regulatory cells by gastrointestinal stimulation as a strategy for asthma control. Mucosal immunology. http://www.citeulike.org/user/HEIRS/article/7560150
Chapman, J. T., Otterbein, L. E., Elias, J. A., and Choi, A. M. K. (2001). Carbon monoxide attenuates aeroallergen-induced inflammation in mice. Am J Physiol Lung Cell Mol Physiol, 281(1):L209-216. http://www.citeulike.org/user/HEIRS/article/7560177
Zhou, X., Kong, N., Zou, H., Brand, D., Li, X., Liu, Z., and Zheng, S. G. G. (2010). Therapeutic potential of tgf-beta-induced cd4(+) foxp3(+) regulatory t cells in autoimmune diseases. Autoimmunity. http://www.citeulike.org/user/HEIRS/article/7560254
Fousteri, G., Dave, A., Bot, A., Juntti, T., Omid, S., and von Herrath, M. (2010). Subcutaneous insulin b:9-23/ifa immunisation induces tregs that control late-stage prediabetes in nod mice through il-10 and ifngamma. Diabetologia, 53(9):1958-1970. http://www.citeulike.org/user/HEIRS/article/7299083

Ultrafine particles in air pollution may heighten allergic inflammation in asthma

"Ultrafine particles in air pollution may heighten allergic inflammation in asthma UCLA-led study has implications for traffic-related asthma flares......A new academic study led by UCLA scientists has found that even brief exposure to ultrafine pollution particles near a Los Angeles freeway is potent enough to boost the allergic inflammation that exacerbates asthma."

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Toluene regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma.

Concept: Toluene is a chemical that needs to be handled correctly to prevent occupational injury.

New study suggests therapeutic approaches to elevate HO-1/Ferritin through the Nrf2 pathway may help alleviate symptoms from exposure to toluene.

Read more about: HO-1 tag in the library and on the Blog: Tag HO-1.















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CiteULike: Toluene diisocyanate (TDI) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma.: "Kim, S.-H. H., Choi, G.-S. S., Ye, Y.-M. M., Jou, I., Park, H.-S. S., and Park, S. M. (2010). Toluene diisocyanate (tdi) regulates haem oxygenase-1/ferritin expression: implications for toluene diisocyanate-induced asthma. Clinical and experimental immunology."

Formaldehyde linked to asthma

Formaldehyde linked to asthma: "URL: Formaldehyde linked to asthma

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TLR-related pathway analysis: novel gene–gene interactions in the development of asthma and atopy

TLR-related pathway analysis: novel gene–gene interactions in the development of asthma and atopy: "URL: TLR-related pathway analysis: novel gene–gene interactions in the development of asthma and atopy

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Asthma and genes encoding components of the vitamin D pathway

Genetic variants at the vitamin D receptor (VDR) locus are associated with asthma and atopy. We hypothesized that polymorphisms in other genes of the vitamin D pathway are associated with asthma or atopy.

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Traffic-related air pollution associated with poor asthma scores

Traffic-related air pollution associated with poor asthma scores

Passive smoking is a major determinant of exhaled nitric oxide levels in allergic asthmatic children

Passive smoking is a major determinant of exhaled nitric oxide levels in allergic asthmatic children

Hyaluronic acid dsyregulation implicated in COPD, asthma

Hyaluronic acid dsyregulation implicated in COPD, asthma