The role of interleukin-33 in chronic rhinosinusitis

Kim, Dong Kyu; Jin, Hong; Eun, Kyoung Mi; Mo, Ji‐Hun; Cho, Seong H.; Oh, Sohee; Cho, David; Kim, Dae Woo

doi:10.1136/thoraxjnl-2016-208772

Cited by 103 publications

(86 citation statements)

References 36 publications

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“…CRSsNP and CRSwNP show distinct inflammatory endotypes with CRSwNP being associated with increased levels of tissue IL‐5, tissue eosinophilia, and concomitant asthma . IL‐33 was upregulated in nasal polyp tissues from patients with CRSwNP as compared with those of CRSsNP or healthy control subjects . Furthermore, IL‐33 mRNA expression in nasal biopsy specimens was higher in CRSwNP patients, in particular those who were resistant to treatment .…”

Section: Il‐33 In Human Airway Diseasesmentioning

confidence: 96%

IL‐33: biological properties, functions, and roles in airway disease

Drake

Kita

2017

Immunological Reviews

202

203

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Summary Interleukin (IL)-33 is a key cytokine involved in type 2 immunity and allergic airway diseases. Abundantly expressed in lung epithelial cells, IL-33 plays critical roles in both innate and adaptive immune responses in mucosal organs. In innate immunity, IL-33 and group 2 innate lymphoid cells (ILC2s) provide an essential axis for rapid immune responses and tissue homeostasis. In adaptive immunity, IL-33 interacts with dendritic cells, Th2 cells, follicular T cells, and regulatory T cells, where IL-33 influences the development of chronic airway inflammation and tissue remodeling. The clinical findings that both the IL-33 and ILC2 levels are elevated in patients with allergic airway diseases suggest that IL-33 plays an important role in the pathogenesis of these diseases. IL-33 and ILC2 may also serve as biomarkers for disease classification and to monitor the progression of diseases. In this article, we reviewed the current knowledge of the biology of IL-33 and discussed the roles of the IL-33 in regulating airway immune responses and allergic airway diseases.

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Section: Il‐33 In Human Airway Diseasesmentioning

confidence: 96%

IL‐33: biological properties, functions, and roles in airway disease

Drake

Kita

2017

Immunological Reviews

202

203

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“…The study by Kim et al , published in Thorax , assessed lL-33 expression at the protein and message level with correlations to differential groups of proinflammatory cells and cytokine expression in Korean subjects with CRSwNP and CRSsNP versus normal control 13. This study found that IL-33 expression is increased in two mucosal sites: NP and uncinate process from CRS and that IL-33 immunostaining is colocalised to CD68+ macrophage.…”

mentioning

confidence: 89%

Role of interleukin 33 in chronic rhinosinusitis

Sehmi

2017

Thorax

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“…A significant up-regulation of ST2 expression has been demonstrated in ethmoid mucosa from CRSwNP, but the concentration of IL-33 protein is not significantly different between nasal polyp and control tissue 31. Kim et al23 have recently demonstrated that IL-33 is up-regulated in other CRS tissues compared to eosinophilic NP and correlates with Th1/Th17 cytokines. IL-33 may contribute to the induction of different types of inflammation under various microenvironments.…”

Section: Pathogenesis and Endotypes Of Crsmentioning

confidence: 99%

“…Epithelial-derived innate cytokines, such as interleukin (IL)-25, IL-33, and TSLP, may also participate in the evolution of NP 22. IL-33 is secreted by immune cells, such as macrophages and dendritic cells as well as epithelial cells 23. Full-length IL-33 is extracellularly released when epithelial cells undergo necrosis and necroptosis via tissue damage caused by external stimuli.…”

Section: Pathogenesis and Endotypes Of Crsmentioning

confidence: 99%

Emerging Endotypes of Chronic Rhinosinusitis and Its Application to Precision Medicine

Kim

Cho

2017

Allergy Asthma Immunol Res

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Chronic rhinosinusitis (CRS) is a heterogeneous inflammatory disease with various underlying pathophysiologic mechanisms which translate to endotypes, in contrast to clinical phenotypes or histological subtypes. Defining endotypes can help clinicians predict disease prognosis, select subjects suitable for a specific therapy, and assess risks for comorbid conditions, including asthma. Therefore, with recent advancement of biologicals in CRS clinical trials, endotyping can be a breakthrough in treating recalcitrant CRS. CRS is caused by dysregulated immunologic responses to external stimuli, which induce various inflammatory mediators from inflammatory cells, including innate lymphoid cells (ILCs) and T lymphocytes as well as epithelial cells. Thymic stromal lymphopoietin (TSLP), interleukin (IL)-25, and IL-33, which are mainly secreted by epithelial cells in response to external stimuli, act on type 2 ILCs and T helper 2 (Th2) cells, inducing IL-4, IL-5, and IL-13. Local immunoglobulin E (IgE) production is also a signature event in nasal polyps (NP). These inflammatory mediators are novel potential therapeutic targets for recalcitrant CRS. This article reviews recent publications regarding endotypes and endotype-based therapeutic strategies in CRS and NP.

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The role of interleukin-33 in chronic rhinosinusitis

Abstract: Our data suggest a role for IL-33 in the pathogenesis of CRSwNP via neutrophil recruitment. Therefore, anti-IL-33 may provide a new treatment strategy to target infiltrating neutrophils in CRSwNP.

Cited by 103 publications

References 36 publications

IL‐33: biological properties, functions, and roles in airway disease

IL‐33: biological properties, functions, and roles in airway disease

Role of interleukin 33 in chronic rhinosinusitis

Emerging Endotypes of Chronic Rhinosinusitis and Its Application to Precision Medicine

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