Alpha2B-Adrenergic Receptor Regulates Neutrophil Recruitment in MSU-Induced Peritoneal Inflammation

Duan, Lihua; Chen, Jie; Razavi, Michael; Wei, Yingying; Ying, Tao; Rao, Xiaoquan; Zhong, Jixin

doi:10.3389/fimmu.2019.00501

Cited by 13 publications

(8 citation statements)

References 36 publications

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“…GLP-1R expression was not affected by treatment with a GLP-1R agonist. IL-1b is believed to be a critical proinflammatory cytokine in the pathogenesis of gout, and exerts a wide range of systemic and local effects (22). In humans, IL-1b production by resident macrophages is stimulated by MSU crystals, and plays a crucial role in the pathogenesis of gout (30).…”

Section: Discussionmentioning

confidence: 99%

“…The inflammatory response to monosodium urate (MSU) crystals triggers macrophage and neutrophil recruitment, leading to the symptoms of an acute gout attack. Intraperitoneal injection of MSU crystals in mice is used as an animal model of gout that can mimic acute episodes of gout (22). Following exposure to MSU, macrophages acquire a proinflammatory M1 phenotype instead of an antiinflammatory M2 phenotype (23,24).…”

Section: Introductionmentioning

confidence: 99%

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Glucagon-Like Peptide-1 Receptor Regulates Macrophage Migration in Monosodium Urate-Induced Peritoneal Inflammation

et al. 2022

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Glucagon-like peptide-1 (GLP-1) is an insulinotropic peptide that signals through the GLP-1 receptor (GLP-1R). GLP-1R, therefore, plays a critical role in diabetes and cardiovascular disease. Whether GLP-1R is involved in inflammatory disease such as gout remains unclear. Macrophages are critical effector cells in the pathogenesis of gout, a common form of inflammatory arthritis caused by the deposition of uric acid in joints. The expression of GLP-1R at the protein level is controversial due to the lack of specificity of existing antibodies against GLP-1R. Using a transgenic mouse model expressing enhanced green fluorescent protein (EGFP) under the control of GLP-1R promoter, here we confirmed the expression of GLP-1R by macrophages. M2 type macrophages and Ly6C+ macrophages expressed higher levels of GLP-1R, compared to their counterparts. GLP-1R deficient macrophages displayed a reduced the migratory ability and an enhanced expression of interleukin (IL)-6, while the expression of IL-1β was not affected. In monosodium urate (MSU) crystal-induced peritonitis, an experimental model of gout, the recruitment of macrophages, especially M2 macrophages, was significantly suppressed in GLP-1R knockout mice compared to wild-type mice. In conclusion, our data suggests that GLP-1R plays a critical role in macrophage migration in MSU-induced inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Glucagon-Like Peptide-1 Receptor Regulates Macrophage Migration in Monosodium Urate-Induced Peritoneal Inflammation

et al. 2022

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“…The MSU-induced peritonitis model was used to investigate the inhibitory effects of Crocin on NLRP3-mediated inflammation. The intraperitoneal injection of MSU leads to NLRP3 inflammasome-dependent peritonitis, which is characterized by IL-1β and IL-18 production and the neutrophil influx into the peritoneal cavity [ 28 ]. Mice were pre-treated with Crocin for 2 h, followed by an intraperitoneal injection of MSU.…”

Section: Resultsmentioning

confidence: 99%

Crocin Attenuates NLRP3 Inflammasome Activation by Inhibiting Mitochondrial Reactive Oxygen Species and Ameliorates Monosodium Urate-Induced Mouse Peritonitis

Sangare

Madhi

Kim

et al. 2023

CIMB

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Crocin is a hydrophilic carotenoid pigment found in the stigma of Crocus sativus or the fruit of Gardenia jasminoides. In this study, we investigated the effects of Crocin on the activation of the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain containing 3 (NLRP3) inflammasome in J774A.1 murine macrophage cells and monosodium urate (MSU)-induced peritonitis. Crocin significantly inhibited Nigericin-, adenosine triphosphate (ATP)-, MSU-induced interleukin (IL)-1β secretion, and caspase-1 cleavage without affecting pro-IL-1β and pro-caspase-1. Crocin also suppressed gasdermin-D cleavage and lactate dehydrogenase release and enhanced cell viability, indicating that Crocin reduces pyroptosis. Similar effects were observed in primary mouse macrophages. However, Crocin did not affect poly(dA:dT)-induced absent in melanoma 2 (AIM2) and muramyl dipeptide-induced NLRP1 inflammasomes. Crocin decreased Nigericin-induced oligimerization and the speck formation of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC). Crocin also dramatically alleviated the ATP-induced production of mitochondrial reactive oxygen species (mtROS). Finally, Crocin ameliorated the MSU-induced production of IL-1β and IL-18 and the recruitment of neutrophils during peritoneal inflammation. These results suggest that Crocin suppresses NLRP3 inflammasome activation by blocking mtROS production and ameliorates MSU-induced mouse peritonitis. Thus, Crocin may have therapeutic potential in various NLRP3 inflammasome-related inflammatory diseases.

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“…In an experimental arthritic animal model, EPI can lower the expression of TNF-alpha, IL-1β, and IL-6 ( 32 ). However, alpha adrenergic receptors are important in neutrophil migration and peritoneal tissue inflammation caused by monosodium urate crystals ( 33 ). These examples demonstrate that catecholamines can have a variety of tissue- and condition-specific effects.…”

Section: Stress As a Stimulator Of Neuroimmune Cross-talk Processmentioning

confidence: 99%

A Hypothesis Regarding Neurosecretory Inhibition of Stress Mediators by Colchicine in Preventing Stress-Induced Familial Mediterranean Fever Attacks

Korkmaz

Cansu²

2022

Front. Immunol.

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Familial Mediterranean fever (FMF) is a monogenic autoinflammatory disease characterized by recurrent episodes of fever and serositis. Colchicine (Col) has a crucial role in the prevention of amyloidosis and FMF attacks. The effect of Col on innate immune cells is based on the inhibition of the microtubule system. The microtubule system is also very important for neurosecretory functions. The inhibitory effect of Col on neurosecretory functions is an overlooked issue. Considering that the neuroimmune cross-talk process plays a role in the development of inflammatory diseases, the effect of Col on the neuronal system becomes important. FMF attacks are related to emotional stress. Therefore, the effect of Col on stress mediators is taken into consideration. In this hypothetical review, we discuss the possible effects of Col on the central nervous systems (CNS) and peripheral nervous systems (PNS) in light of mostly experimental study findings using animal models. Studies to be carried out on this subject will shed light on the pathogenesis of FMF attacks and the other possible mechanisms of action of Col apart from the anti-inflammatory features.

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Alpha2B-Adrenergic Receptor Regulates Neutrophil Recruitment in MSU-Induced Peritoneal Inflammation

Cited by 13 publications

References 36 publications

Glucagon-Like Peptide-1 Receptor Regulates Macrophage Migration in Monosodium Urate-Induced Peritoneal Inflammation

Glucagon-Like Peptide-1 Receptor Regulates Macrophage Migration in Monosodium Urate-Induced Peritoneal Inflammation

Crocin Attenuates NLRP3 Inflammasome Activation by Inhibiting Mitochondrial Reactive Oxygen Species and Ameliorates Monosodium Urate-Induced Mouse Peritonitis

A Hypothesis Regarding Neurosecretory Inhibition of Stress Mediators by Colchicine in Preventing Stress-Induced Familial Mediterranean Fever Attacks

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