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Role of Interleukin 33 in Chronic Rhinosinusitis

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Role of Interleukin 33 in Chronic Rhinosinusitis Thorax Online First, published on February 27, 2017 as 10.1136/thoraxjnl-2016-209655 Editorial Thorax: first published as 10.1136/thoraxjnl-2016-209655 on 27 February 2017. Downloaded from identified as a ligand for the orphan IL-1 Role of interleukin 33 in chronic family receptor, suppression of tumori- genicity 2 (ST2; also known as IL-1RL1, rhinosinusitis T1, IL-33R) expressed on monocytes, mast cells, eosinophils, Th2 cells and Roma Sehmi ILC2. IL-33 exerts its cytokine activity by binding to a heterodimer of ST2 and co-receptor, IL-1 receptor accessory Chronic rhinosinusitis (CRS) is a heter- discrepancies over which isoforms of protein. IL-33 is a chromatin-associated ogenous airways disease characterised by TGF-β are increased per se and in what nuclear cytokine and as such is expressed inflammation of the upper airways and racial populations of CRSsNP, INF-γ is constitutively at high levels in the nuclei sinuses that persists for at least 12 weeks. elevated. Since CRSsNP is diagnosed by of various human and mouse tissues at CRS is frequently divided into two endo- the absence of NPs, it is by definition steady state, including endothelial, epithe- types based on the presence or absence heterogenous and thus the outcome of lial and fibroblast-like cells.9 This nuclear of nasal polyps (NPs): CRS with NPs these studies is heavily influenced by the expression can be further increased (CRSwNP) and CRS without NPs population sampled.4 Accurate subclassifi- during inflammatory conditions, viral (CRSsNP). Inflammatory patterns in the cations will be necessary to determine infection and cigarette smoke. IL-33 does two groups are different and studies indi- more accurately the inflammatory pattern not contain a signal sequence and there- cate that CRSsNP is dominated by a type 1 in each group. fore is not secreted as a conventional inflammatory profile associated with in- Inflammation in CRSwNP is charac- cytokine. Instead, it functions as an creased interferon (INF)-γ and tumour ne- terised by type 2 inflammation and inc- endogenous danger signal or nuclear crosis factor (TGF)-β expression and reased tissue eosinophilia compared with alarmin that is released after cell injury to neutrophilic inflammation.1 By compari- CRSsNP or control sinus mucosa. Type 2 alert the immune system of damage son, type 2 inflammatory responses charac- cytokines, IL-5 and IL-13, can be pro- during trauma or infection. Once released terised by interleukin (IL) 4, IL-5, IL-13 duced by several immune cells including the bioactive isoforms of IL-33 can stimu- cytokine expression and eosinophilic in- T helper two cells, mast cells and group 2 late type 2 cytokine production by ILC2 flammation are features of CRSwNP.1 This innate lymphoid cells (ILC2). IL-5 pro- and IL-13 production by macrophages categorisation may, however, be oversim- motes local differentiation of eosinophil- which in turn promote a maladaptive plified as recent studies show that this may lineage committed progenitors and TH2inflammatory response that is be subject to racial and regional differ- increased activation and prolonged sur- IgE-independent and may explain the clin- ences.23While the majority of Caucasian vival of mature eosinophils, IL-13 acti- ical observation that many patients with patients sampled in the USA and Europe vates macrophages, B cells and epithelial CRSwNP are non-allergic (figure 1).4 have a pronounced infiltration of eosino- cells to release chemoattractants that in- IL-33 expression has been shown to be phils and expression of IL-5 in the duce recruitment of eosinophils and Th2 increased in cultures of sinonasal epithelial NPs, patients with CRSwNP in East Asian cells and IgE mediated reactions and tissue cells in recalcitrant CRSwNP, and it is countries including Japan, Korea and remodelling.1 In contrast to CRSsNP, further enhanced in a bacteria associated http://thorax.bmj.com/ China, exhibit a mixed inflammatory fibrin deposition in the submucosa of NPs molecular pattern.10 In addition, other profile. About half the Asian patients with is especially high and thought to represent studies have shown that expression of ST2 CRSwNP exhibit an eosinophilic chronic a key event in the tissue remodelling is increased in the ethmoid sinus mucosa rhinosinusitis (ECRS) while the rest have a process of CRSwNP.4 Several studies have of CSRwNP compared with CRSsNP.11 non-eosinophilic more neutrophilic or now shown that the inflammatory profile Similarly, in subjects with CRS with mixed inflammatory chronic rhinosinusitis of CRSwNP varies among racial groups eosinophilic NPs, increased ST2 levels (non-ECRS) characterised by type 1 dom- although the exact aetiology of these dif- were detected at the mRNA and protein inant inflammation. Although a number of ferences remains to be clarified. It is levels, compared with non-eosinophilic on September 29, 2021 by guest. Protected copyright. hypotheses have been proposed regarding undeniable that this may also reflect a lack CRS and normals. The levels of IL-33 the pathogenesis of CRSwNP, the precise of international consensus for defining mRNA were however not different molecular mechanisms remain unclear and tissue eosinophilia. While some groups between these groups12 and correlation of likely lie beyond rudimentary clinical clas- define eosinophilia as an absolute number the cytokine expression to various proin- sifications of CRS. An emphasis on defin- of eosinophils (five to eight) per random flammatory cell types was not investigated. ing CRS endotypes based on distinct high powered field,356others use a The study by Kim et al, published in functional or pathobiological mechanisms cut-off percentage of eosinophils (5–15%) Thorax, assessed lL-33 expression at the of disease may be more effective at identi- for a number of high power fields protein and message level with correla- fying patient groups that would respond to counted in areas of greatest cellularity.78 tions to differential groups of proinflam- therapeutic interventions targeting specific It has become evident that disruption matory cells and cytokine expression in proinflammatory mediators or infectious of the mucosal interface in response to Korean subjects with CRSwNP and agents that trigger the disease pathology. environmental and microbial stimuli or by CRSsNP versus normal control.13 This The inflammatory profile of CRSsNP cellular damage may drive local inflamma- study found that IL-33 expression is is largely type 1, although there are tory responses. IL-33 is a recently increased in two mucosal sites: NP and described airway epithelial-derived cyto- uncinate process from CRS and that IL-33 kine recognised as a key activator of immunostaining is colocalised to CD68+ Correspondence to Dr Roma Sehmi, innate and adaptive cells that drive type 2 macrophage. Although several studies CardioRespiratory Research Group, Department of Medicine, Health Sciences Building, Rm 3U32, immune responses, contributing to tissue have shown that CD45+ haemopoietic McMaster University, 1200 Main St West, Hamilton, homoeostasis and response to environ- cells can be induced to express IL-33 Ontario, Canada L8N 3Z5; [email protected] mental stresses (figure 1). IL-33 was under inflammatory conditions, the levels Sehmi R. Thorax Month 2017 Vol 0 No 0 1 Copyright Article author (or their employer) 2017. Produced by BMJ Publishing Group Ltd (& BTS) under licence. Editorial Thorax: first published as 10.1136/thoraxjnl-2016-209655 on 27 February 2017. Downloaded from that generated a mixed inflammatory infil- trate, Kim et al showed that anti-IL-33 attenuated polyp formation, neutrophilia and CXCL2 levels but had no effect on eosinophil recruitment and IL-4 levels. As a note of caution, in assessing the role of IL-33 in animal models of disease, species-specific differences should be taken into account. For example, whereas in humans IL-33 is expressed constitu- tively by the lung airway epithelium, in mice it is expressed by alveolar type 2 pneumocytes.16 17 These differences may be important when extrapolating results from mouse models for therapeutic target- ing of IL-33 in human patients. In closing, Kim et al have shown that IL-33 expression is elevated in nasal tissues of patients with CRSwNP, and expression of this cytokine is associated Figure 1 Potential mechanisms for amplification of neutrophilic inflammation in CRSwNP. with Th1/Th17 cytokines, neutrophil Several factors including fungi, proteases, bacteria viruses and allergens can activate nasal recruitment and remodelling. It is likely epithelial cells and resident myeloid dendritic cells (mDCs) to produce alarmin cytokines including that IL-33 is one of the crucial mediators IL-33 which drive maladaptive innate type 2 inflammatory responses. IL-33 stimulates resident of pathogenesis in CRSwNP through neu- group 2 innate lymphoid to secrete IL-4, IL-5 and IL-13 in an allergen non-specific manner which promotes dysregulated type 2 immune responses. mDCs activation also promotes naive CD4+ T trophil recruitment, but further study is cell differentiation into Th2 CD4+ T cells, which then further release type 2 cytokines. IL-4 and required to understand if this is a promis- IL-13 induce B cell isotype switching and leads to IgE-mediated reactions through activation of ing target for the treatment of patients basophils and mast cells. Nasal mast cells can also be activated directly by IL-33, leading to with all endotypes of CRSwNP or specific downstream release of cysteinyl leukotrienes (CysLT), which activate ILC2s, and IL-5 and IL-13, to pathobiological initiators of this upper which further contribute to downstream type 2 inflammation. IL-5 production from activated Th2 airway inflammatory condition. CD4+ T cells and ILC2s promote eosinophil recruitment, as well as eotaxin produced by nasal epithelial cells and M2 macrophages. In addition, IL-33 which can indirectly promote neutrophilia Competing interests None declared. by activating resident proinflammatory cells such as M2 macrophages to secrete (1) Provenance and peer review Commissioned; chemoattractants that recruit neutrophils including CXCL2 or (2) produce more IL-33 that prevents externally peer reviewed.
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