Desloratadine Ameliorates Olfactory Disorder and Suppresses AMPA Receptor GluA1 Expression in Allergic Rhinitis Rat

Li, Shenling; Zhang, Xiaotian; Li, Zhiyuan; Jiang, Xiaodan; Zhang, Niankai; Zhang, Jisheng; Huang, Yi‐Chuan; Zhao, Han; Jiang, Yan; Li, Na

doi:10.1007/s00005-020-00569-3

Cited by 6 publications

(8 citation statements)

References 27 publications

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“…It is generally believed that the pathogenesis of ARrelated OD involves a mechanical component (i.e., mucosal congestion blocks the nasal airway) and an inflammatory component. 21 However, studies did not confirm a direct relationship between the degree of nasal obstruction and the AR-related OD. For example, Cowart et al found that although the nasal resistance in AR patients was significantly higher than that in normal controls, it was not related to the changes of olfactory thresholds.…”

Section: Discussionmentioning

confidence: 98%

P2X7 receptor of microglia in olfactory bulb mediates the pathogenesis of olfactory dysfunction in a mouse model of allergic rhinitis

et al. 2023

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The pathogenesis of allergic rhinitis (AR)-related olfactory dysfunction (OD) remains unknown. Inhibiting microglial response in olfactory bulb (OB) can ameliorate AR-related OD, but no precise targets have been available. In this study, we established a mouse model of ovalbumin (OVA)-induced AR and combined with the application of P2X7 receptor (P2X7R)-specific antagonists and cell culture in conditioned medium to investigate the role and mechanism of OB microglial P2X7R in AR-related OD. Serum IgE and IL-5 levels determined via ELISA and federated the number of nose-scratching to affirm the success of OVA-induced AR mouse model. Buried food pellet test was used to evaluate the olfactory function of mice. The changes of IBA1, GFAP, P2X7R, IL-1β, IL-1Ra, and CASPASE 1 were detected by quantitative polymerase chain reaction and western blotting.The levels of adenosine triphosphate (ATP) were determined by the commercialized kit. The morphological changes of microglia were assessed using immunofluorescence staining and Sholl analysis. Findings showed that AR-related OD was associated with OB microglia-mediated imbalance between IL-1β and IL-1Ra. Treatment with BBG improved the olfactory function in AR mice with

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Section: Discussionmentioning

confidence: 98%

P2X7 receptor of microglia in olfactory bulb mediates the pathogenesis of olfactory dysfunction in a mouse model of allergic rhinitis

et al. 2023

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“…Serum level of IL‐17, the key cytokine produced by Th17 cells, was increased in AR patients and correlated to severity of symptoms (Ciprandi et al, 2009). IL‐17 has been shown to induce the activation of allergen‐specific Th2 cell, accumulation of eosinophil and neutrophil, and production of IgE in AR (Li et al, 2020; Quan et al, 2012). Neutralization of IL‐17 by antibodies markedly reduced AR symptoms and decreased both Th2 and Th17 response (Gu et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

IL2‐inducible T‐cell kinase inhibitor ibrutinib reduces symptoms and Th2 differentiation in mouse allergic‐rhinitis model

Liu

Gao

2021

Drug Development Research

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Th2 and Th17 immune response contribute to allergic rhinitis (AR) development. Targeting Th2 and Th17 response has been shown to ameliorate AR. Ibrutinib is an inhibitor for IL2‐inducible T‐cell kinase, which can promote Th2 and Th17 immune response. We sought to investigate the effect of ibrutinib on AR and the underlying mechanisms. We established house dust mite‐induced AR mouse model and treated AR mice with ibrutinib. The symptoms of AR, serum level of immunoglobulin E, percentage of Th1, Th2, Th17, and Treg in nasal lymphoid tissues were monitored. We also established in vitro T cell differentiation cell culture model. The T cells were treated with ibrutinib and the expression of specific transcriptional factors and cytokines was measured. The activation of PLC‐γ1/calcium/NFAT2 signaling pathway was detected. Ibrutinib treatment had no effects on the development of lymphocytes and myeloid cells, but alleviated AR symptoms and decreased Th2 cell population in nasal lymphoid tissue. Meanwhile, iburitnib suppressed Th2 and Th17 differentiation in vitro. Moreover, iburitnib prevented phosphorylation of PLC‐γ1and nuclear translocation of NFAT2 in Th2 cells. Our results suggested that ibrutinib could ameliorate AR symptoms through suppression of Th2 differentiation in AR mouse model.

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“…Varying degrees of apoptosis of nerve cells in the olfactory bulb and olfactory receptors can be induced (Gao et al, 2019; Passali et al, 2021). Moreover, changes in receptors associated with the surface of the olfactory bulb, such as raising number of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolylpropionic acid (AMPA) receptor subunit glutamate receptor 1 (GluR1) and decreased number of glutamate receptor 2 (GluR2) on the surface of the olfactory bulb (Li et al, 2020; Liu et al, 2021), can trigger glutamate transmitter system dysfunction and precipitate the development of olfactory dysfunction. Hao Lv et al revealed that both the level of immune‐inflammation and apoptosis of olfactory neurons were increased in the olfactory bulb of AR mice with olfactory dysfunction.…”

Section: “Nose‐brain Communication” Mechanism Of Ar‐related Neurologi...mentioning

confidence: 99%

Brain response in allergic rhinitis: Profile and proposal

Wang

Song

Wei

et al. 2022

J of Neuroscience Research

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In addition to typical nasal symptoms, patients with allergic rhinitis (AR) will further lead to symptoms related to brain function such as hyposmia, anxiety, depression, cognitive impairment, memory loss, etc., which seriously affect the quality of life of patients and bring a heavy burden to the patient's family and society. Some scholars have speculated that there may be potential “nose‐brain communication” mechanism in AR that rely on neuro‐immunity. This mechanism plays an important role in AR‐associated brain response process. However, no study has directly demonstrated which neural circuits will change in the connection between the nose and brain during the onset of AR, and the mechanism which underlines this question is also lack. Focusing on the topic of “nose‐brain communication”, this paper systematically summarizes the latest research progress between AR and related brain responses and discusses the mechanism of AR‐related neurological phenotypes. Hope new diagnostic and therapeutic targets to ameliorate the brain function‐related symptoms and improve the quality of life of AR patients will be developed.

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Desloratadine Ameliorates Olfactory Disorder and Suppresses AMPA Receptor GluA1 Expression in Allergic Rhinitis Rat

Cited by 6 publications

References 27 publications

P2X7 receptor of microglia in olfactory bulb mediates the pathogenesis of olfactory dysfunction in a mouse model of allergic rhinitis

P2X7 receptor of microglia in olfactory bulb mediates the pathogenesis of olfactory dysfunction in a mouse model of allergic rhinitis

IL2‐inducible T‐cell kinase inhibitor ibrutinib reduces symptoms and Th2 differentiation in mouse allergic‐rhinitis model

Brain response in allergic rhinitis: Profile and proposal

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