We are analyzing https://link.springer.com/article/10.1186/s13075-014-0504-2.

Title:
The sympathetic nervous response in inflammation | Arthritis Research & Therapy
Description:
Over the past decades evidence has accumulated clearly demonstrating a pivotal role for the sympathetic nervous system (SNS) and its neurotransmitters in regulating inflammation. The first part of this review provides the reader with an overview showing that the interaction of the SNS with the immune system to control inflammation is strongly context-dependent (for example, depending on the activation state of the immune cell or neuro-transmitter concentration). In the second part we focus on autoimmune arthritis as a well investigated example for sympathetically controlled inflammation to show that the SNS and catecholamines play a differential role depending on the time point of ongoing disease. A model will be developed to explain the proinflammatory effects of the SNS in the early phase and the anti-inflammatory effects of catecholamines in the later phase of autoimmune arthritis. In the final part, a conceptual framework is discussed that shows that a major purpose of increased SNS activity is nourishment of a continuously activated immune system at a systemic level using energy-rich fuels (glucose, amino acids, lipids), while uncoupling from central nervous regulation occurs at sites of inflammation by repulsion of sympathetic fibers and local adrenoceptor regulation. This creates zones of ‘permitted local inflammation’. However, if this ‘inflammatory configuration’ persists and is strong, as in autoimmunity, the effects are detrimental because of the resultant chronic catabolic state, leading to cachexia, high blood pressure, insulin resistance, and increased cardiovascular mortality, and so on. Today, the challenge is to translate this conceptual knowledge into clinical benefit.
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Keywords {🔍}

pubmed, google, scholar, sympathetic, cells, cas, sns, inflammation, immune, arthritis, system, nervous, inflammatory, antiinflammatory, activity, central, nerve, chronic, local, activation, proinflammatory, cell, increased, figure, response, straub, disease, effects, fibers, model, regulation, influence, release, neurotransmitters, norepinephrine, production, systemic, brain, receptor, role, clinical, level, rheum, high, regulatory, tissue, shown, effect, βars, experimental,

Topics {✒️}

collagen-type ii-induced arthritis tumor growth factor-β tumor necrosis factor/phagocytes pkc/erk dependent pathway bradykinin-induced neurogenic migration cholinergic anti-inflammatory pathway α2-dependent proinflammatory effects hypothalamic-pituitary-adrenal il central nervous system alpha-adrenergic receptor augments central sympatholytic therapy acute carrageenan-induced arthritis hypothalamic–pituitary–adrenal axis target neural-immune pathways sns-dependent monocyte recruitment beta2-adrenergic receptor signaling central nervous sytem catecholamine-producing tyrosine hydroxylase collagen-induced arthritis model nerve growth factor il-10-producing anti-inflammatory human cd4 + cd25+ regulatory catecholamine-producing cells start splenic sympathetic neurons central sympathetic activity tumor necrosis factor �peripheral nervous system vagal nervous system autonomic nervous system article download pdf regional intravenous guanethidine nerve repellent receptor exceptional immune-privileged site sympathetic nervous system murine antigen-induced arthritis gram-negative peritonitis increased anti-inflammatory function local anti-inflammatory mechanisms hypothalamic-pituitary-adrenal �collagen induced arthritis collagen-induced arthritis net anti-inflammatory outcome net anti-inflammatory effect immune-related diseases dominant anti-inflammatory effect authors’ original file full size image privacy choices/manage cookies sensory nervous system sympathetic downstream signaling

Questions {❓}

A prophet unheeded?
Effect of sympathetic dysfunction?
How can one explain this dichotomy?
However, why do some immune cells, like macrophages, express both α-ARs and β-ARs, which will counteract each other in terms of immunoregulation?
Sanders VM: The beta2-adrenergic receptor on T and B lymphocytes: do we understand it yet?

Schema {🗺️}

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      headline:The sympathetic nervous response in inflammation
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         Orthopedics
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