Role of interleukin 33 in chronic rhinosinusitis

Sehmi, Roma

doi:10.1136/thoraxjnl-2016-209655

Cited by 3 publications

(4 citation statements)

References 17 publications

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“…Additionally, another recent study investigating the bidirectional development between sinusitis and IBD reported that the duration of IBD, UC, steroid exposure, and younger age of IBD diagnosis were associated with subsequent sinusitis in patients with UC, whereas steroid exposure and duration of sinusitis were significantly associated with subsequent IBD in patients with sinusitis [ 25 ]. For these reasons, we hypothesize that UC and CRSsNP have been intrinsically associated with a network of deregulated inflammatory mediators, such as the interleukin (IL)-33/ST2 pathway [ 26 , 27 , 28 , 29 ]. IL-33 is one of the major innate cytokines involved in the pathophysiology of CRS in Asian populations.…”

Section: Discussionmentioning

confidence: 99%

Could Chronic Rhinosinusitis Increase the Risk of Ulcerative Colitis? A Nationwide Cohort Study

Lee

Son

et al. 2022

Diagnostics

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Chronic rhinosinusitis (CRS) is a common chronic inflammatory disease of the sinonasal mucosa with an inflammatory or infectious etiology. Inflammatory bowel disease (IBD) causes chronic intestinal inflammation. Thus, both diseases share innate immune and epithelial barrier dysfunctions of the mucosa. However, the association between sinusitis and IBD is not well-known. We aimed to determine the association between CRS and the risk for IBDs, such as Crohn’s disease (CD) and ulcerative colitis (UC). In this long-term retrospective cohort study, 15,175 patients with CRS and 30,350 patients without CRS (comparison group) were enrolled after 1:2 propensity score matching. The incidence rates of CD and UC were 0.22 and 0.51 (1000 person-years), respectively. The adjusted hazard ratio (HR) for developing CD and UC in CRS patients was 1.01 (95% confidence interval (CI), 0.66–1.54) and 1.72 (95% CI, 1.26–2.36), respectively. Additionally, in the subgroup analysis using the CRS phenotype, the adjusted HRs of UC were significantly increased in patients with CRS without nasal polyps (adjusted HR = 1.71; 95% CI, 1.24–2.35), but not in those with CRS with nasal polyps. CRS without nasal polyps is associated with an increased incidence of UC but not CD. Therefore, clinicians should pay attention to the early detection of UC when treating patients with CRS without nasal polyps.

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Section: Discussionmentioning

confidence: 99%

Could Chronic Rhinosinusitis Increase the Risk of Ulcerative Colitis? A Nationwide Cohort Study

Lee

Son

et al. 2022

Diagnostics

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“…76 IL-33, an airway epithelium-derived nuclear cytokine belonging to the IL-1 family, is constitutionally expressed in the epithelial cells of nasal polyps. 77 In the presence of IL-33, Th2 cells can synthesize more IL-5 and IL-13, which is a key activator driving type 2 immune response. 78 Hajime et al 79 found that IL-33 can induce mucin gene expression and goblet cell proliferation in human nasal epithelial cells, and the specific mechanism remains to be further studied.…”

Section: Tnf-α and Mucinmentioning

confidence: 99%

“…IL‐31 synergizes with IL‐4 or IL‐13 to induce MUC5AC gene expression in HM3‐MUC5AC cells and human airway A549 cells 76 . IL‐33, an airway epithelium‐derived nuclear cytokine belonging to the IL‐1 family, is constitutionally expressed in the epithelial cells of nasal polyps 77 . In the presence of IL‐33, Th2 cells can synthesize more IL‐5 and IL‐13, which is a key activator driving type 2 immune response 78 .…”

Section: Characteristics Of Mucin Hypersecretion In Different Endotyp...mentioning

confidence: 99%

Characteristics of mucin hypersecretion in different inflammatory patterns based on endotypes of chronic rhinosinusitis

Zhai,

Shao,

et al. 2024

Clinical & Translational All

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BackgroundChronic rhinosinusitis (CRS) is usually accompanied by mucin hypersecretion that can lead to mucus accumulation and impair nasal mucociliary clearance, thus exacerbating airway inflammation. Abnormal mucin hypersecretion is regulated by different T helper (Th) cytokines, which are associated with different endotype‐driven inflammatory responses. Therefore, it is of great significance to understand how these factors regulate mucin hypersecretion to provide precise treatment strategies for different endotypes of CRS.BodyThus far, the most common endotypes of CRS are classified as type 1, type 2, or type 3 immune responses based on innate and adaptive cell‐mediated effector immunity, and the representative Th cytokines in these immune responses, such as IFN‐γ, TNF‐α, IL‐4, IL‐5, IL‐13, IL‐10, IL‐17, and IL‐22, play an important regulatory role in mucin secretion. We reviewed all the related literature in the PubMed database to determine the expression of these Th cytokines in CRS and the role they play in the regulation of mucin secretion.ConclusionWe believe that the main Th cytokines involved in specific endotypes of CRS play a key role in regulating abnormal mucin secretion, which contributes to better understanding of the pathogenesis of CRS and provides therapeutic targets for airway inflammatory diseases associated with mucin hypersecretion.

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“…The IL‐33 receptor is a heterodimeric complex of suppression of tumorigenicity 2 (ST2) and IL‐1 receptor accessory protein, which is expressed on various immune cells, including Th2 cells, eosinophils, macrophages, mast cells, basophils and natural killer cells. Therefore, the release of IL‐33 is recognized as a key activator of innate and adaptive cells that drive Th2 immune responses . Recently, IL‐33 is also noted for its role in regulating the function of type 2 innate lymphoid cells (ILC), a heterogeneous family of cells of lymphoid morphology that produce IL‐13 in response to IL‐33 stimulation.…”

Section: Precision Medicine In Crsmentioning

confidence: 99%

Novel findings in immunopathophysiology of chronic rhinosinusitis and their role in a model of precision medicine

Ong

Wang

2019

Allergy

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Our understanding of the pathophysiology of chronic rhinosinusitis (CRS) is continuously evolving. The traditional description of CRS in terms of two phenotypes based on the presence or absence of nasal polyps belies the underlying intricate immunopathophysiological processes responsible for this condition. CRS is being increasingly recognized as a disease spectrum encompassing a range of inflammatory states in the sinonasal cavity, with non-type 2 inflammatory disease on one end, type 2 inflammatory, eosinophil-heavy disease on the other and an overlap of both in different proportions in between. Abundance in research on the immune mechanisms of CRS has revealed various new endotypes that hold promise as biomarkers for the development of targeted therapies in severe, uncontrolled CRS. The introduction of precision medicine to manage this chronic, complex condition is a step forward in providing individualized care for all patients with CRS. In this review, the latest research on the pathophysiology of CRS with a focus on potential novel biomarkers and treatment options over the last 2 years are summarized and integrated into a suggested model of precision medicine in CRS. K E Y W O R D S biomarkers, chronic rhinosinusitis, endotypes, immunopathophysiology, precision medicine

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Role of interleukin 33 in chronic rhinosinusitis

Cited by 3 publications

References 17 publications

Could Chronic Rhinosinusitis Increase the Risk of Ulcerative Colitis? A Nationwide Cohort Study

Could Chronic Rhinosinusitis Increase the Risk of Ulcerative Colitis? A Nationwide Cohort Study

Characteristics of mucin hypersecretion in different inflammatory patterns based on endotypes of chronic rhinosinusitis

Novel findings in immunopathophysiology of chronic rhinosinusitis and their role in a model of precision medicine

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