Restraint stress increased the permeability of the nasal epithelium in BALB/c mice

Jarillo-Luna, Rosa Adriana; Gutiérrez-Meza, Juan Manuel; Franco-Vadillo, Antonio; Rivera-Aguilar, Víctor; Toledo-Blas, Mireille; Cárdenas-Jaramillo, Luz María

doi:10.1016/j.psyneuen.2020.104700

Cited by 4 publications

(4 citation statements)

References 42 publications

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“…31,32 Many studies have shown that stress generally increases gut permeability, regardless of the type or location of stress. 33 The mechanism of increased intestinal permeability due to stress remains unclear, but CRH, mast cells, functional changes in the cannabinoid type 1 receptor, and the modification and redistribution of TJ proteins are reported to be involved. In this study, we found that the expression of ZO-1 and JAM-A was decreased, while that of Claudin 2 was increased.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, not only does the gut microbiota imbalance caused by stress lead to changes in the intestinal barrier, but chronic stress itself also alters the maintenance of the structural integrity of the mucosal barrier 31,32 . Many studies have shown that stress generally increases gut permeability, regardless of the type or location of stress 33 . The mechanism of increased intestinal permeability due to stress remains unclear, but CRH, mast cells, functional changes in the cannabinoid type 1 receptor, and the modification and redistribution of TJ proteins are reported to be involved.…”

Section: Discussionmentioning

confidence: 99%

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The effect of occlusal disharmony on a chronic stress‐induced animal model of gut microbiota dysbiosis

Zhang

et al. 2022

J of Oral Rehabilitation

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Background and Objectives: Chronic stress (CS) is closely related to intestinal health.Occlusal disharmony (OD) is a risk factor for hypersensitivity to novel stress, and the relationship between OD and the intestinal system with or without other chronic stresses remains unclear. Therefore, the purpose of this study was to investigate whether OD affects the gut microbiota and the intestinal barrier in a CS-exposed animal model. Methods: OD was induced by making a 0.5-mm-thick incision on the right maxillary molar. CS involved exposure to one stressor per day for 35 days. Sprague-Dawley rats were randomly divided into an untreated control group and OD-, CS-and OD + CStreated groups. The behavioural tests, serum corticosterone level, gut microbiota composition and tight junction protein expression in colon tissue were measured on the 56th day to elucidate the effect of OD on animals under CS. Results: Significant differences in performance on behavioural tests and serum corticosterone concentrations were observed on day 56 in the OD + CS group compared with the control group. Exposure to occlusal disharmony or chronic stress resulted in a change in the composition of the gut microbiota of rats. Differences in the expression of the tight junction proteins zonula occludens-1 and junctional adhesion molecule-A were observed in colon tissue from the OD + CS group compared with the control group. Conclusions: We concluded that the significant changes in performance on behavioural tests, serum corticosterone concentrations and microbiota dysbiosis and tight junction protein levels induced by OD with CS may indicate that OD is a potential factor promoting gut microbiota dysbiosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The effect of occlusal disharmony on a chronic stress‐induced animal model of gut microbiota dysbiosis

Zhang

et al. 2022

J of Oral Rehabilitation

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“…It has long been appreciated that psychological stress may trigger or aggravate allergic rhinitis and other allergic diseases, [1][2][3][4][5] however, the underlying mechanisms are poorly understood. Although allergic rhinitis impairs patients' quality of life, and prenatal maternal psychological stress might even predispose to postnatal rhinorrhea and nasal inflammation in the offspring, 6,7 there is no specific treatment for stress-aggravated nasal allergy.…”

Section: Introductionmentioning

confidence: 99%

Corticotropin-releasing hormone stimulates mast cell degranulation and proliferation in human nasal mucosa

Yamanaka-Takaichi,

Mizukami,

Sugawara

et al. 2024

Preprint

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Background: Psychological stress exacerbates mast cell (MC)-dependent inflammation, including nasal allergy, but the underlying mechanisms are not well understood. Because the key stress-mediating neurohormone, corticotropin-releasing hormone (CRH), induces human skin MC degranulation, we hypothesized that CRH may be a key player in stress-aggravated nasal allergy. The current study probes this hypothesis in human nasal mucosa MCs (hM-MCs) in situ, using nasal polyp organ culture, and tests whether CRH is required for murine M-MC activation by perceived stress in vivo. Methods: Organ-cultured nasal polyps were used as a surrogate tissue for human upper airway mucosa and stimulated with CRH. In addition to quantitative immunohistomorphometry and transmission electron microscopy, we investigated whether perceived (restraint) stress activates murine M-MCs in vivo and whether this is CRH-dependent. Results: CRH stimulation significantly increased the number of hM-MCs, stimulated both their degranulation and proliferation ex vivo, and increased SCF expression in human nasal mucosa epithelium compared to controls. CRH also sensitized hM-MCs to further CRH stimulation and promoted a pro-inflammatory hM-MC phenotype. The CRH-induced increase in hM-MCs was abrogated by co-administration of CRH-R1 specific antagonist antalarmin, CRH-R1 siRNA, or SCF-neutralizing antibody. In vivo, both acute and chronic restraint stress significantly increased the number and degranulation of murine M-MCs compared to sham-stressed mice. This effect was abrogated by intranasal antalarmin. Conclusion: CRH is a major activator of hM-MC in nasal mucosa, in part via promoting SCF production, and CRH-R1 antagonists like antalarmin are promising candidate therapeutics for nasal mucosa neuroinflammation induced by perceived stress.

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“…It has long been appreciated that psychological stress may trigger or aggravate allergic rhinitis and other allergic diseases [1][2][3][4][5]; however, the underlying mechanisms are poorly understood. Although allergic rhinitis impairs patients' quality of life, and prenatal maternal psychological stress might even predispose the offspring to postnatal rhinorrhea and nasal inflammation [6,7], there is no specific treatment for stress-aggravated nasal allergy.…”

Section: Introductionmentioning

confidence: 99%

Stress and Nasal Allergy: Corticotropin-Releasing Hormone Stimulates Mast Cell Degranulation and Proliferation in Human Nasal Mucosa

Yamanaka‐Takaichi

Mizukami

Sugawara

et al. 2021

IJMS

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Psychological stress exacerbates mast cell (MC)-dependent inflammation, including nasal allergy, but the underlying mechanisms are not thoroughly understood. Because the key stress-mediating neurohormone, corticotropin-releasing hormone (CRH), induces human skin MC degranulation, we hypothesized that CRH may be a key player in stress-aggravated nasal allergy. In the current study, we probed this hypothesis in human nasal mucosa MCs (hM-MCs) in situ using nasal polyp organ culture and tested whether CRH is required for murine M-MC activation by perceived stress in vivo. CRH stimulation significantly increased the number of hM-MCs, stimulated both their degranulation and proliferation ex vivo, and increased stem cell factor (SCF) expression in human nasal mucosa epithelium. CRH also sensitized hM-MCs to further CRH stimulation and promoted a pro-inflammatory hM-MC phenotype. The CRH-induced increase in hM-MCs was mitigated by co-administration of CRH receptor type 1 (CRH-R1)-specific antagonist antalarmin, CRH-R1 small interfering RNA (siRNA), or SCF-neutralizing antibody. In vivo, restraint stress significantly increased the number and degranulation of murine M-MCs compared with sham-stressed mice. This effect was mitigated by intranasal antalarmin. Our data suggest that CRH is a major activator of hM-MC in nasal mucosa, in part via promoting SCF production, and that CRH-R1 antagonists such as antalarmin are promising candidate therapeutics for nasal mucosa neuroinflammation induced by perceived stress.

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Restraint stress increased the permeability of the nasal epithelium in BALB/c mice

Cited by 4 publications

References 42 publications

The effect of occlusal disharmony on a chronic stress‐induced animal model of gut microbiota dysbiosis

The effect of occlusal disharmony on a chronic stress‐induced animal model of gut microbiota dysbiosis

Corticotropin-releasing hormone stimulates mast cell degranulation and proliferation in human nasal mucosa

Stress and Nasal Allergy: Corticotropin-Releasing Hormone Stimulates Mast Cell Degranulation and Proliferation in Human Nasal Mucosa

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