The Role of Transforming Growth Factor-α on Mucin Overproduction in Eosinophilic Chronic Rhinosinusitis

Ishinaga, Hajime; Shah, Said Ahmad; Sakaida, Hiroshi; Takeuchi, Kazuhiko

doi:10.1159/000333794

Cited by 9 publications

(11 citation statements)

References 35 publications

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“…MUC5AC is one of the major respiratory mucins and has been shown to be induced by a wide variety of stimuli, including not only pro-inflammatory cytokines [11], epidermal growth factor receptor (EGFR) ligand [20], and bacterial pathogens [11,12], but also Th2 cytokines, including IL-4, IL-9, and IL-13 [16,17,18]. Mucus hypersecretion is one of the major symptoms in allergic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Effects of Interleukin-31 on MUC5AC Gene Expression in Nasal Allergic Inflammation

et al. 2013

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Background: Interleukin-31 (IL-31) is a newly discovered T helper lymphocyte-derived cytokine that plays an important role in allergic inflammation. However, the effects of IL-31 on mucus production in nasal allergic inflammation are completely unknown. Objective: To investigate the effects of IL-31 on mucin gene expression (MUC5AC) in patients with allergic rhinitis and in human airway epithelial cells. Methods: Expression levels of IL-31 and IL-31 receptor A (IL-31RA) were evaluated in the inferior turbinate of patients with allergic rhinitis and non-allergic rhinitis with immunohistochemistry. IL-31-induced MUC5AC gene expression was measured with a MUC5AC luciferase reporter assay in human epithelial HM3-MUC5AC cells and quantified by quantitative real-time polymerase chain reaction in human airway epithelial A549 cells. Results: IL-31RA was primarily localized in submucosal glands and upregulated in allergic rhinitis. IL-31 was detected in submucosal tissue and increased in allergic inflammation. MUC5AC gene expression was induced by IL-31 stimulation both in HM3-MUC5AC and A549 cells. Additionally, IL-31 cooperated with Th2 cytokines on MUC5AC gene expression in HM3-MUC5AC cells. Conclusion: IL-31 and IL-31RA are upregulated in patients with allergic rhinitis, and induce MUC5AC gene expression in human airway epithelial cells. These findings suggest that IL-31 plays an important role in mucus overproduction in nasal allergic inflammation.

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Section: Discussionmentioning

confidence: 99%

Effects of Interleukin-31 on MUC5AC Gene Expression in Nasal Allergic Inflammation

et al. 2013

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“…Patients with ECRS present with loss of smell, long-term nasal congestion, thick mucus production, and intermittent acute exacerbation of secondary bacterial infections. The quality of life of these patients is severely impaired [ 2 ]. ECRS is a subtype of chronic sinusitis that is thought to occur secondarily to systemic eosinophil deregulation [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…Patients with ECRS show a strong possibility of overlapping mechanisms for eosinophilia and have a poor response to medical and surgical management. Therefore, ECRS is considered to be a refractory and intractable disease [ 2 ]. Several stimuli, including fungal antigens, allergens, bacteria, and bacteria-derived superantigens, may be involved in the pathophysiology of ECRS [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Pathogenesis of eosinophilic chronic rhinosinusitis

2016

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Eosinophilic chronic rhinosinusitis (ECRS) is considered a refractory and intractable disease. Patients with ECRS present with thick mucus production, long-term nasal congestion, loss of sense of smell, and intermittent acute exacerbations secondary to bacterial infections. Despite medical and surgical interventions, there is a high rate of recurrence with significant impairment to quality of life. The recent increasing prevalence of ECRS in south Asian countries and the strong tendency of ECRS to reoccur after surgery should be considered. The majority of cases need repeat surgery, and histological examinations of these cases show eosinophilic-dominant inflammation. The degradation and accumulation of eosinophils, release of cytokines, and mucus secretion have important roles in the pathogenesis of ECRS. ECRS differs from non-ECRS, in which eosinophils are not involved in the pathogenesis of the disease, and also in terms of many clinical characteristics, blood examination and nasal polyp histological findings, clinical features of the disease after surgery, efficacy of medications, and computed tomography findings. This review describes the clinical course, diagnosis, and treatment of ECRS as well as its pathophysiology and the role of eosinophils, mucus, cytokines, and other mediators in the pathogenesis of ECRS.

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“…Accordingly, ECRS is considered a refractory and intractable disease. 23 In the present study, we specifically enrolled an uncontrolled ECRS subpopulation and evaluated GPR17 and CysLT1R levels in polyp tissues. We found a significant difference in the…”

Section: Discussionmentioning

confidence: 99%

Expression of cysteinyl leukotriene receptor GPR17 in eosinophilic and non-eosinophilic chronic rhinosinusitis with nasal polyps

Chen

Yang

et al. 2017

Asian Pac J Allergy Immunol

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Background: The cysteinyl leukotrienes (cysLTs) are proinflammatory lipid mediators that act on the type 1 cysLT receptor (CysLT1R) in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP). GPR17, a G protein-coupled orphan receptor with homology to the cysLT receptors, has been proposed as a damage sensor during inflammation. However, the expression and correlation of GPR17 and CysLT1R in eosinophilic CRSwNP (ECRS) and non-eosinophilic CRSwNP (non-ECRS) have not been well investigated.

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The Role of Transforming Growth Factor-α on Mucin Overproduction in Eosinophilic Chronic Rhinosinusitis

Cited by 9 publications

References 35 publications

Effects of Interleukin-31 on MUC5AC Gene Expression in Nasal Allergic Inflammation

Effects of Interleukin-31 on MUC5AC Gene Expression in Nasal Allergic Inflammation

Pathogenesis of eosinophilic chronic rhinosinusitis

Expression of cysteinyl leukotriene receptor GPR17 in eosinophilic and non-eosinophilic chronic rhinosinusitis with nasal polyps

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