Neuro-immune interactions in the cholinergic anti-inflammatory reflex.

Immunol Lett

University of California Davis, School of Veterinary Medicine, Department of Anatomy, Physiology, and Cell Biology, 1089 Veterinary Medicine Drive, VM3B, Room 2007, Davis, CA 95616, United States. Electronic address:

Published: October 2016

Communication between the nervous and immune systems can significantly alter immune cell function in a number of inflammatory diseases. Elegant studies have defined a basic functional circuit in a "cholinergic anti-inflammatory pathway" that highlights a unique role for the vagus nerve, and has brought about a resurgence in the field of neuro-immunology. This research has further identified that in addition to tonic signals that can restrain immune cell activation; the anti-inflammatory reflex arc is amiable to targeted stimulation as a therapeutic modality. The success of vagal electrical neural stimulation in a plethora of pre-clinical inflammation models has spurred the development of "electroceuticals" or neurostimulatory devices in the treatment of chronic inflammation. This development has begun despite addressing of fundamental questions such as the functional neural circuitry being crudely mapped and unresolved mechanisms of action of acetylcholine on target immune cells. Perhaps fortuitously, rapid advances in neuroscience techniques may allow us to begin to answer some of these longstanding questions and clarify recent controversies.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.imlet.2016.08.006DOI Listing

Publication Analysis

Top Keywords

anti-inflammatory reflex
8
immune cell
8
neuro-immune interactions
4
interactions cholinergic
4
cholinergic anti-inflammatory
4
reflex communication
4
communication nervous
4
immune
4
nervous immune
4
immune systems
4

Similar Publications

Article Synopsis
  • The pathogenesis of long COVID (LC) involves uncertainty, complicating the search for effective therapies.
  • The hypothesis suggests that chronic damage to the body's anti-inflammatory mechanisms, particularly through the vagus nerve, HPA axis, and mitochondrial function, plays a crucial role in LC development.
  • The theory posits that SARS-CoV-2 alters these systems at various levels, leading to persistent inflammation due to impaired anti-inflammatory responses from acetylcholine and cortisol, warranting further investigation into glucocorticoid receptor sensitivity and potential long-term epigenetic effects.
View Article and Find Full Text PDF

Growing evidence reveals that microglia activation and neuroinflammatory responses trigger cell loss in the brain. Histamine is a critical neurotransmitter and promotes inflammatory responses; thus, the histaminergic system is a potential target for treating neurodegenerative processes. JNJ-7777120, a histamine H4 receptor (HR) antagonist, has been shown to alleviate inflammation, brain damage, and behavioral deficits effectively, but there is no report on its role in brain trauma.

View Article and Find Full Text PDF

DBI/ACBP is a phylogenetically ancient hormone that stimulates appetite and lipo-anabolism. In response to starvation, DBI/ACBP is secreted through a noncanonical, macroautophagy/autophagy-dependent pathway. The physiological hunger reflex involves starvation-induced secretion of DBI/ACBP from multiple cell types.

View Article and Find Full Text PDF

Dermatomyositis is a multi-system, connective tissue immune-mediated inflammatory condition characterised by myositis and distinct skin manifestations, with a higher prevalence in women. Symptoms typically appear in adulthood, though a juvenile form exists. Early signs may include Gottron's papules and heliotrope rash, with proximal muscle weakness as the second most common initial symptom.

View Article and Find Full Text PDF

The cardinal clinical features of complex regional pain syndrome type I (CRPS-I) are pain, edema, autonomic changes, and limitation of motoric movement, which may indicate the role of inflammation and cytokines. We report the effect of prednisolone on the clinical severity and mRNA profiling of proinflammatory (tumor necrosis factor (TNF)-α and interleukin (IL)-2) and anti-inflammatory cytokines (IL-10 and transforming growth factor (TGF)-β) in the patient with CRPS-I. Thirty-nine patients with CRPS-I of shoulder joint were enrolled.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!