Hutan
Senior Member
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There was an announcement on Australian ABC radio today that a Monash university team have found that autoimmunity is a significant cause of treatment resistant hypertension. (I think other teams have been working on this idea too).
'Furthermore, blocking antibody production by depletion of B cells, protects mice against the development of hypertension.'
It's interesting given that autoimmunity has been implicated in POTS and of course Fluge and Mella's theory about endothelial dysfunction. Hypertension is such a big money spinner for drug companies. Perhaps this will result in much more research that helps ME patients.
This, from the university website, gives some background.
http://www.med.monash.edu.au/pharmacology/docs/pharmacology-honours-projects-2016.pdf
'Furthermore, blocking antibody production by depletion of B cells, protects mice against the development of hypertension.'
It's interesting given that autoimmunity has been implicated in POTS and of course Fluge and Mella's theory about endothelial dysfunction. Hypertension is such a big money spinner for drug companies. Perhaps this will result in much more research that helps ME patients.
This, from the university website, gives some background.
http://www.med.monash.edu.au/pharmacology/docs/pharmacology-honours-projects-2016.pdf
UNDERSTANDING THE IMMUNE BASIS OF HYPERTENSION
Supervisor: A/Prof Grant Drummond, Prof Chris Sobey Location: Vascular Biology & Immunopharmacology Group
Department of Pharmacology Monash University, Clayton
Background: Hypertension is a major cause of heart failure, heart attacks and strokes. Over 4 million Australians have hypertension and alarmingly, in up to 50% of cases, the condition is not controlled by current medications. Recent research has led to the recognition that hypertension is associated with activation of the immune system and accumulation of leukocytes (e.g. T cells, B cells and macrophages) in organs such as the kidneys, arteries and brain. Such findings suggest that immune-modulating therapies – akin to those already used to treat autoimmune disease – could be employed to control high blood pressure, especially in patients who do not respond to current drugs. But first, we must develop a better understanding of the factors that modulate the immune system in hypertension, and the mechanisms by which activated leukocytes promote inflammation and damage to arteries, kidneys and the brain.
Project 1: Does the gut microbiome influence sensitivity to hypertension? Disturbances to the make-up of gut bacteria, caused by diet or drugs (e.g. antibiotics), can influence health and disease. Thus, we wish to explore the role of the gut microbiome in regulation of immunity during hypertension. In this project, the gut microbiome of healthy mice will be manipulated by feeding them specialized diets or by co-housing them with hypertensive mice (mice eat each other’s poo!) to determine whether their sensitivity to hypertension is altered.
Project 2: How do B cells and autoantibodies cause hypertension? Hypertension in humans is associated with raised levels of circulating antibodies. We have shown that this also occurs in mouse models and that these antibodies accumulate in the walls of arteries. Furthermore, blocking antibody production by depletion of B cells, protects mice against the development of hypertension. We now wish to determine the targets (i.e. antigens) of antibodies in the vessel wall and investigate how antibodies interact with leukocytes, particularly macrophages, to cause their activation and the subsequent release of cytokines that promote vascular inflammation and stiffening.