Neural regulation of gastrointestinal inflammation: Role of the sympathetic nervous system

Cervi, Andrea; Lukewich, Mark K.; Lomax, Alan E.

doi:10.1016/j.autneu.2013.12.003

Cited by 58 publications

(35 citation statements)

References 102 publications

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“…On the other hand, the muscularis macrophages regulate the enteric neurons and peristalsis. Furthermore, it is found that subpopulations of B‐cells, neutrophils, and macrophages, specifically muscularis macrophages, express a large number of β 2 adrenergic receptors (Cervi et al, ). It is also well described in the literature that alpha adrenergic signaling boosts inflammation, while beta adrenergic signaling suppresses both innate and adaptive immunity (del Rey and Besedovsky, ; Guereschi et al, ).…”

Section: Catecholaminesmentioning

confidence: 99%

Neurotransmitters: The Critical Modulators Regulating Gut–Brain Axis

Mittal

Debs

Patel

et al. 2017

Journal Cellular Physiology

450

287

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Neurotransmitters including catecholamines and serotonin play a crucial role in maintaining homeostasis in the human body. Studies on these neurotransmitters mainly revolved around their role in the “fight or flight” response, transmitting signals across a chemical synapse and modulating blood flow throughout the body. However, recent research has demonstrated that neurotransmitters can play a significant role in the gastrointestinal (GI) physiology. Norepinephrine (NE), epinephrine (E), dopamine (DA), and serotonin have recently been a topic of interest because of their roles in the gut physiology and their potential roles in gastrointestinal and central nervous system pathophysiology. These neurotransmitters are able to regulate and control not only blood flow, but also affect gut motility, nutrient absorption, gastrointestinal innate immune system, and the microbiome. Furthermore, in pathological states such as inflammatory bowel disease (IBD) and Parkinson’s disease, the levels of these neurotransmitters are dysregulated, therefore causing a variety of gastrointestinal symptoms. Research in this field has shown that exogenous manipulation of catecholamine serum concentrations can help in decreasing symptomology and/or disease progression. In this review article, we discuss the current state-of-the-art research and literature regarding the role of neurotransmitters in regulation of normal gastrointestinal physiology, their impact on several disease processes, and novel work focused on the use of exogenous hormones and/or psychotropic medications to improve disease symptomology.

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Section: Catecholaminesmentioning

confidence: 99%

Neurotransmitters: The Critical Modulators Regulating Gut–Brain Axis

Mittal

Debs

Patel

et al. 2017

Journal Cellular Physiology

450

287

View full text Add to dashboard Cite

show abstract

“…For example, imbalances in this symbiotic relationship have been associated with diverse diseases, such as obesity, nervous system disorders, chronic kidney disease, inflammatory bowel disease (IBD), and CVD 14, 15 . However, the involvement of the host-gut relationship in hypertension has yet to be investigated in detail despite the fact that: (i) The gut is the most highly innervated peripheral organ, with significant numbers of the motor fibers to the gut identified as sympathetic nerves 16 . It is pertinent to note that elevated sympathetic nervous system activity is a hallmark of both animal and human hypertension 8, 9 ; (ii) ANS influences gut permeability 17 , inflammatory state 18 , and microbial communities in IBD and other diseases 19 ; (iii) gut microbial products, such as short chain fatty acids (SCFAs), lipopolysaccharides (LPS), and neurotransmitters influence both the immune and vascular systems 20, 21 ; and (iv) studies from our group and others have demonstrated a link between gut dysbiosis and hypertension 22, 23 .…”

Section: Introductionmentioning

confidence: 99%

Hypertension-Linked Pathophysiological Alterations in the Gut

Santisteban¹,

Qi²,

Zubcevic³

et al. 2017

Circulation Research

424

421

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Rationale Sympathetic nervous system control of inflammation plays a central role in hypertension. The gut receives significant sympathetic innervation, is densely populated with a diverse microbial ecosystem, and contains immune cells that greatly impact overall inflammatory homeostasis. Despite this uniqueness, little is known about the involvement of the gut in hypertension. Objective Test the hypothesis that increased sympathetic drive to the gut is associated with increased gut wall permeability, increased inflammatory status, and microbial dysbiosis and that these gut pathological changes are linked to hypertension. Methods and Results Gut epithelial integrity and wall pathology were examined in spontaneously hypertensive rat (SHR) and chronic Angiotensin II infusion rat models. The increase in blood pressure in SHR was associated with gut pathology that included increased intestinal permeability and decreased tight junction proteins. These changes in gut pathology in hypertension were associated with alterations in microbial communities relevant in blood pressure control. We also observed enhanced gut-neuronal communication in hypertension originating from paraventricular nucleus of the hypothalamus and presenting as increased sympathetic drive to the gut. Finally, angiotensin converting enzyme inhibition (captopril) normalized blood pressure and was associated with reversal of gut pathology. Conclusions A dysfunctional sympathetic-gut communication is associated with gut pathology, dysbiosis, and inflammation, and plays a key role in hypertension. Thus, targeting of gut microbiota by innovative probiotics, antibiotics, and fecal transplant, in combination with current pharmacotherapy, may be a novel strategy for hypertension treatment.

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“…Given this strategic location, they might play an important role in regulating antigen processing and presentation. In a mouse model of infectious colitis, activation of β3 adrenergic receptors decreased the production of proinflammatory cytokines . Similarly, in a mouse model of S. typhimurium infection, treatment with a β adrenergic receptor agonist increased mouse survival rates by decreasing TNF‐α and increasing IL‐10 levels in serum, while treatment with an α adrenergic receptor agonist led to opposite effects .…”

Section: Efferent Interactionsmentioning

confidence: 96%

Catecholamines and acetylcholine are key regulators of the interaction between microbes and the immune system

Weinstein

Revuelta

Hernández-Pando

2015

Annals of the New York Academy of Sciences

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Recent studies suggest that catecholamines (CAs) and acetylcholine (ACh) play essential roles in the crosstalk between microbes and the immune system. Host cholinergic afferent fibers sense pathogen-associated molecular patterns and trigger efferent cholinergic and catecholaminergic pathways that alter immune cell proliferation, differentiation, and cytokine production. On the other hand, microbes have the ability to produce and degrade ACh and also regulate autogenous functions in response to CAs. Understanding the role played by these neurotransmitters in host-microbe interactions may provide valuable information for the development of novel therapies.

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Neural regulation of gastrointestinal inflammation: Role of the sympathetic nervous system

Cited by 58 publications

References 102 publications

Neurotransmitters: The Critical Modulators Regulating Gut–Brain Axis

Neurotransmitters: The Critical Modulators Regulating Gut–Brain Axis

Hypertension-Linked Pathophysiological Alterations in the Gut

Catecholamines and acetylcholine are key regulators of the interaction between microbes and the immune system

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