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Cholinergic anti-inflammatory pathway and its role in cardiovascular disease

Research group

Active research

Project owner

Institute for neuroscience and physiology

Area

Health and

medicine

Topic

Basic

Medicine

Physiology

Short description

Cardiovascular disease, manifested as myocardial infarction and/or stroke, is the leading cause of death in the world. The underlying factor for cardiovascular disease is usually atherosclerosis. Inflammation is central in cardiovascular disease, not only for the pathogenesis of atherosclerosis, but also in complications following atherosclerosis, for example during and after embolus/thrombus formation. The long-term goal of our research is to identify novel targets for the treatment and prevention of inflammation associated with cardiovascular disease. Our hypothesis is that the autonomic nervous system and the immune system interacts, and that nerve signalling can modulate inflammation. By combining experimental models with human material we can investigate these interactions from several different perspectives.

Our research

Cardiovascular disease, manifested as myocardial infarction and/or stroke, is the leading cause of mortality and morbidity globally. The underlying factor for cardiovascular disease is usually atherosclerosis. Inflammation is central in cardiovascular disease, not only for the pathogenesis of atherosclerosis, but also in complications following atherosclerosis, for example during and after embolus/thrombus formation (ischemia-reperfusion injury). The autonomic nervous system can modulate inflammation in acute inflammatory models. If this also occurs in cardiovascular disease is not known.

In this research project we address the interaction between autonomic nervous system and inflammation, focusing on the cholinergic alpha 7 nicotinic acetylcholine receptor (a7nAChR) signaling and identifying the mechanisms of a7nAChR action and how it mediates its anti-inflammatory effects in atherosclerosis and in ischemia-reperfusion injury in the brain (stroke) and heart (myocardial infarction). We have recently shown that the a7nAChR is expressed in human carotid plaques and that lack of a7nAChR dramatically accelerates atherosclerosis (Johansson ME et al ATVB 2014) whereas stimulation of the a7nAChR decreases atherosclerosis (Ulleryd MU Atherosclerosis 2019). By combining experimental models and human material we will identify the mechanisms whereby the a7nAChR modulates inflammation and thereby influences the development of atherosclerosis and ischemia-reperfusion brain injury.