Role of adrenergic receptor signalling in neuroimmune communication

Chhatar, Sushanta; Lal, Girdhari

doi:10.1016/j.crimmu.2021.11.001

Cited by 55 publications

(19 citation statements)

References 234 publications

(233 reference statements)

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“…Our study has several limitations. Firstly, α 2 adrenergic receptors are expressed on both immune and nonimmune cells [ 62 ]. In the present study, we only observed the outcomes of the lung after DEX intervention but did not explore how DEX affects the function of various immune cells.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Protects against Airway Inflammation and Airway Remodeling in a Murine Model of Chronic Asthma through TLR4/NF-κB Signaling Pathway

Zhou

Wang

et al. 2023

Mediators of Inflammation

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Asthma is a common respiratory disease characterized by chronic airway inflammation. Dexmedetomidine (DEX), a highly selective α2 adrenergic receptor agonist, has been shown to participate in regulating inflammatory states and thus exert organ protective actions. However, the potential of DEX in asthma is still unknown. This study is aimed at investigating the role of DEX in a mouse model of house dust mite- (HDM-) induced asthma and exploring its underlying mechanism. Here, we found that DEX treatment significantly ameliorated airway hyperresponsiveness, airway inflammation, and airway remodeling in the asthmatic mice, which were similar to the efficacy of the reference anti-inflammatory drug dexamethasone. In addition, DEX reversed the increased expression of toll-like receptor 4 (TLR4) and its downstream signaling adaptor molecule nuclear factor-κB (NF-κB) in the lung tissue of asthmatic mice. Furthermore, these protective effects of DEX were abolished by yohimbine, an α2 adrenergic receptor antagonist. These results indicate that DEX is capable of ameliorating airway inflammation and remodeling in asthmatic mice, and this protective effect is associated with the inhibition of the TLR4/NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Protects against Airway Inflammation and Airway Remodeling in a Murine Model of Chronic Asthma through TLR4/NF-κB Signaling Pathway

Zhou

Wang

et al. 2023

Mediators of Inflammation

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“…In contrast to the current findings, b-AR rather than a 1 -AR was thought to mediate the potent antiinflammatory effects of PE. However, what must be emphasized is that PE is considered as a specific a 1 -AR agonist in clincal and basic research (58). Thus, we chose PE to study the effects of a 1 -AR on ARDS.…”

Section: Discussionmentioning

confidence: 99%

α1-adrenoceptor stimulation ameliorates lipopolysaccharide-induced lung injury by inhibiting alveolar macrophage inflammatory responses through NF-κB and ERK1/2 pathway in ARDS

Cong

Yang²,

Zeng³

et al. 2023

Front. Immunol.

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IntroductionCatecholamines such as norepinephrine or epinephrine have been reported to participate in the development of acute respiratory distress syndrome (ARDS) by activating adrenergic receptors (ARs). But the role of α1-AR in this process has yet to be elucidated.MethodsIn this study, ARDS mouse model was induced by intratracheal instillation of lipopolysaccharide. After treatment with α1-AR agonist phenylephrine or antagonist prazosin, lung pathological injury, alveolar barrier disruption and inflammation, and haemodynamic changes were evaluated. Cytokine levels and cell viability of alveolar macrophages were measured in vitro. Nuclear factor κB (NF-κB), mitogen-activated protein kinase, and Akt signalling pathways were analysed by western blot.ResultsIt showed that α1-AR activation alleviated lung injuries, including reduced histopathological damage, cytokine expression, and inflammatory cell infiltration, and improved alveolar capillary barrier integrity of ARDS mice without influencing cardiovascular haemodynamics. In vitro experiments suggested that α1-AR stimulation inhibited secretion of TNF-α, IL-6, CXCL2/MIP-2, and promoted IL-10 secretion, but did not affect cell viability. Moreover, α1-AR stimulation inhibited NF-κB and enhanced ERK1/2 activation without significantly influencing p38, JNK, or Akt activation.DiscussionOur studies reveal that α1-AR stimulation could ameliorate lipopolysaccharide-induced lung injury by inhibiting NF-κB and promoting ERK1/2 to suppress excessive inflammatory responses of alveolar macrophages.

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“…It is likely that peripheral and/or central potentiation of neural cholinergic signaling with these AchE Inhibitors leads to the engagement of a different neuro-immune pathway and/or effector molecules that control inflammation. For example, galantamine can potentiate the adrenals and autonomic ganglia to release catecholamines (Akiyama et al 2003), which have been shown to suppress inflammation by acting directly on immune cells as effector molecules (Chhatar and Lal 2021;McKinley et al 2022;Murray et al 2021). Future work will focus on identifying the circuits and molecules at play in this model.…”

Section: Discussionmentioning

confidence: 99%

Galantamine attenuates autoinflammation in a mouse model of familial mediterranean fever

Mughrabi

Ochani

Tanovic

et al. 2022

Mol Med

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Background Autoinflammatory diseases, a diverse group of inherited conditions characterized by excessive innate immune activation, have limited therapeutic options. Neuroimmune circuits of the inflammatory reflex control innate immune overactivation and can be stimulated to treat disease using the acetylcholinesterase inhibitor galantamine. Methods We tested the efficacy of galantamine in a rodent model of the prototypical autoinflammatory disease familial Mediterranean fever (FMF). Multiple chronic disease markers were evaluated in animals that received long-term galantamine treatment compared to vehicle. Results Long-term treatment with galantamine attenuated the associated splenomegaly and anemia which are characteristic features of this disease. Further, treatment reduced inflammatory cell infiltration into affected organs and a subcutaneous air pouch. Conclusions These findings suggest that galantamine attenuates chronic inflammation in this mouse model of FMF. Further research is warranted to explore the therapeutic potential of galantamine in FMF and other autoinflammatory diseases.

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Role of adrenergic receptor signalling in neuroimmune communication

Cited by 55 publications

References 234 publications

Dexmedetomidine Protects against Airway Inflammation and Airway Remodeling in a Murine Model of Chronic Asthma through TLR4/NF-κB Signaling Pathway

Dexmedetomidine Protects against Airway Inflammation and Airway Remodeling in a Murine Model of Chronic Asthma through TLR4/NF-κB Signaling Pathway

α1-adrenoceptor stimulation ameliorates lipopolysaccharide-induced lung injury by inhibiting alveolar macrophage inflammatory responses through NF-κB and ERK1/2 pathway in ARDS

Galantamine attenuates autoinflammation in a mouse model of familial mediterranean fever

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