TNF alpha and Chronic Disease.
March 30, 2011 10 Comments
TNF alpha is critical to most chronic illnesses. Regulating its overexpression is critical – but we are designed to have some TNF alpha all the time, and a whole lot when we need it. So we will need to find ways to determine its proper balance. I think we have that available to us in our proper use of biomarkers of inflammation.
In this graphic the researchers bring our attention to the important subject of sensitizing cells to the TNF effect. I believe this is at the heart of the downward spiral of chronic illnesses.
IMMUNE REGULATION OF ALZHEIMER’S AND DIABETES
This link is to an important presentation by the researcher working on the Enbrel® protocol for and therapy for Alzheimer’s. TBI and Stroke. It may be equally important in autism. Please go to the link and click on the video and then listen to his talk. It is important to what I will be talking about in the next series of blogs http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2100099/
And this literature points to the very complex regulatory role of NF- kappa B. It is influenced by TNF and also regulates TNF.
“TNF-α is one of the most prominent pro-inflammatory cytokines significantly increased in AD and it plays a central role in initiating and regulating the cytokine cascade during inflammatory responses. For example, TNF-α increases the expression of adhesion
molecules on the vascular endothelium, which allows leukocytes and immune cells to infiltrate areas of tissue damage and infection.” (I. Granic et al. / NF-κB in Alzheimer’s Disease and Diabetes).
IMMUNE REGULATION OF VASCULAR DISEASE
This quote from Blood Journal illustrates the complexity of the immune regulation of vascular disease. “Atherosclerosis is an inflammatory disease of the arterial wall that carries an important socioeconomic burden. The severe clinical manifestations of atherosclerosis (myocardial infarction, stroke) are mainly due to the abrupt obstruction of the vessel lumen by a thrombus formed on the contact of a ruptured or eroded atherosclerotic plaque. The available data strongly suggest that immunoinflammatory–related mechanisms are the major determinants of plaque complications. Therefore, most of the important advances in the comprehension of the mechanisms of atherosclerosis have come from studies aimed at elucidating the critical components involved in the modulation of the immunoinflammatory balance within the plaque. However, despite the increasing knowledge regarding the role of inflammation in atherogenesis, the precise intracellular transduction pathways involved in this process remain largely unexplored.” (http://bloodjournal.hematologylibrary.org/content/103/3/754.2.full)
Over the next weeks I will be pulling the facts together so you can make better health decisions about all these chronic illnesses including Cancer and HIV and most neurological problems.