Any chance someone could summarize this in bullet point style (just the main points) for those of us whose brains go into tailspins trying to understand this?
I'm taking a lunch break from my duties and thought I'd read the paper to give me something interesting to think about when I have to return.
I'll just summarise the excerpt - no time to read the whole paper.
This is about how acetylcholine (ACh) can affect the immune system.
First they remind us that ACh is an important neurotransmitter in the brain and is the principle neurotransmitter carrying signals from the brain to the periphery via the vagus nerve (ie efferent signals - this is very relevant to the experiments they describe).
There are two types of ACh receptors and the authors note that RNA for both types (ie the message that would result in production of the receptor protein) has been found in various immune and non-immune cytokine-producing cells which themselves produce ACh. In other words ACh is not confined to the nervous system.
They have identified one type of receptor on macrophages and go on to describe experiments with human macrophages in culture.
They show that ACh can significantly reduce production of various proinflammatory cytokines when macrophages are stimulated with endotoxin. Most notable among these is TNF which is an important mediator of the devastating effects of endotoxin. In other words, ACh has a strong anti-inflammatory/immunosuppressive effect.
They then go on to study whether immunosuppressive effects can be observed in the whole animal. For this they use rats with various manipulations of the vagus nerve to increase or decrease ACh production.
Again they show that increase of ACh profoundly suppresses TNF production in response to endotoxin.
Finally they remind us that stimulation of the vagus nerve can lead to anti-inflammatory effects at distant sites and that there is widespread distribution of vagal efferents throughout the reticuloendothelial system and periphery, with signalling along these pathways being very rapid.
They conclude that the cholinergic pathway is uniquely positioned to modulate inflammation in real time.