Nasal diseases and psychological distress

Wang, Deping; Luo, Wenlong

doi:10.1080/13548506.2015.1051064

Cited by 7 publications

(3 citation statements)

References 53 publications

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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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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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“…Previous articles have investigated the association between upper airway pathologies and neuropsychological symptoms [ 6 , 7 ]. In addition, there were several retrospective cohort studies assessing depression and dementia in patients with obstructive sleep apnea (OSA) [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Association of nasal septal deviation with the incidence of anxiety, depression, and migraine: A national population-based study

Lee

Kim

et al. 2021

PLoS ONE

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Background & aims Nasal obstruction caused by nasal septal deviation is very bothersome and, therefore, can affect the patient’s emotional state. However, little is known about the effect of nasal septal deviation (NSD) on the neuropsychiatric aspects of patients. Therefore, this study aims to verify the higher incidence of anxiety, depression, and migraine in patients diagnosed with NSD compared to general populations using big data. Methods This retrospective cohort study collected subjects from the Korean National Health Insurance Service (NHIS) database. Adjustments were made to minimize the confounding of variables for age, sex, residence type, income levels, hypertension, diabetes, dyslipidemia, rhinitis, and chronic rhinosinusitis between the two groups. The primary endpoint of this study was newly diagnosed anxiety, depression, and migraine between January 2009 and December 2018. Kaplan-Meier survival curves, logarithmic rank test, and Cox proportional regression test were used for statistical analysis. Results Among a total of 135,769 subjects in the NHIS database, 48,495 patients with NSD (NSD group) and 54,475 control subjects (control group) were selected. Patients with NSD had an increased risk of anxiety, depression, and migraine compared to the control group. In the NSD group, the adjusted hazard ratios (HR) were 1.236 (95% CI, 1.198–1.276) for anxiety, 1.289 (95% CI, 1.238–1.343) for depression, and 1.251 (95% CI, 1.214–1.290) for migraine. Conclusion NSD is associated with a higher incidence of anxiety, depression, and migraine. Therefore, it is suggested that physicians carefully consider psychoneurological distress and employ therapeutic strategies to minimize these conditions.

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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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Nasal diseases and psychological distress

Cited by 7 publications

References 53 publications

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

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

Association of nasal septal deviation with the incidence of anxiety, depression, and migraine: A national population-based study

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

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