Nasal IL-25 predicts the response to oral corticosteroids in chronic rhinosinusitis with nasal polyps

Hong, Haiyu; Chen, Fenghong; Sun, Yueqi; Yang, Qintai; Gao, Wenxiang; Cao, Yujie; Fan, Yunping; Shi, Jianbo; Li, Hua-Bin

doi:10.1016/j.jaci.2017.10.050

Cited by 25 publications

(15 citation statements)

References 9 publications

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“…However, the potential sources of such local IL-25 accumulation in CRSwNP patients remain relatively uncharacterized, especially given that IL-25 levels can differ between patients. 29 Respiratory viral infections are increasingly associated with chronic allergic and inflammatory diseases since their presence often exacerbates the type 2 inflammation in inflamed airways – despite their conventional activation of type 1 inflammation for viral clearance. 16 , 18 , 24 , 30 , 31 Therefore, to investigate the ability of viral infections to induce expression of IL-25 that is strongly associated with type 2 inflammation, we infected in vitro differentiated hNECs from control and CRSwNP donors, and quantitatively characterized the induction of IL-25.…”

Section: Discussionmentioning

confidence: 99%

Induction of IL-25 Expression in Human Nasal Polyp Epithelium by Influenza Virus Infection is Abated by Interferon-Alpha Pretreatment

Hong

Tan

Yan

et al. 2021

JIR

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Background Epithelial cytokines including IL-25, IL-33 and thymic stromal lymphopoietin (TLSP) are recently established as drivers of type 2 chronic inflammatory diseases such as chronic rhinosinusitis with nasal polyps (CRSwNP). Here, we further confirmed the increased expression of IL-25 in CRSwNP and investigated potential contributors of IL-25 in CRSwNP epithelium. Methods Sixty CRSwNP, 25 CRSsNP and 15 healthy control tissues were examined for IL-25 expression and for the accompanying type 2 inflammatory cytokines. We then tested different respiratory virus infections on human nasal epithelial cells (hNECs) for their ability to trigger IL-25 expression. In addition, we subjected hNECs generated from CRSwNP tissues to pretreatment with recombinant interferon-alpha (IFN-α) prior to viral infection to evaluate IFN effects on IL-25 induction. Results We confirmed that significantly enhanced levels of IL-25 were observed in CRSwNP tissues, and that IL-25 expression correlated with type 2 inflammatory cytokine expression. In vitro, we observed significantly elevated IL-25 in hNECs infected with influenza A virus as early as 24 hours post-infection (hpi), regardless of tissue origin, and IL-25 correlated positively with viral load. While other respiratory viruses exhibited increasing trends of IL-25, these were not significant at the time-points tested. IFN-α treatment of CRSwNP epithelium was found to exert bimodal effects, ie IFN-α treatment alone induced moderate IL-25 expression, whereas IFN-α pretreatment of hNECs before influenza infection significantly diminished IL-25 induction by active influenza virus infection. Conclusion We have authenticated the observation of elevated IL-25 in CRSwNP, which is correlated with type 2 inflammatory cytokines. Notably, we identified influenza virus infection as a potential contributor of IL-25 in both control and CRSwNP epithelium during active infection. This IL-25 induction can be abated by IFN-α pretreatment which ameliorated active influenza infection. Trial Registration Chictr.org.cn ChiCTR-BON-16010179, Registered 18 December 2016, http://www.chictr.org.cn/showproj.aspx?proj=17331 . The authors agree on the sharing of deidentified participant data where it pertains to request directly related to the data in this article when contacted (Haiyu Hong; honghy@mail.sysu.edu.cn ).

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Section: Discussionmentioning

confidence: 99%

Induction of IL-25 Expression in Human Nasal Polyp Epithelium by Influenza Virus Infection is Abated by Interferon-Alpha Pretreatment

Hong

Tan

Yan

et al. 2021

JIR

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“…Patients with NP IL‐25‐high had greater computed tomography (CT) sinus severity scores, worse endoscopy manifestations, and higher type 2‐cytokine levels 27 . Furthermore, NP tissue IL‐25 levels can be applied as a biomarker for predicting the clinical efficacy of oral‐corticosteroid sensitivity and an indicator for concomitant asthma in patients with CRSwNP 46,47 . Similarly, Cheng et al investigated the role of IL‐25 in the lower airway with bronchoscopy and biopsies from asthma patients 48 .…”

Section: Epithelium‐derived Il‐25mentioning

confidence: 99%

“…IL‐25 functions as a master regulator that mediates both innate and adaptive via a combined activation of ILC2s and Th2 cells to evoke sustained Th2‐skewed mucosal inflammation. Recently, Hong and Chen et al found that nasal IL‐25 plays a vital role in promoting Th2‐biased inflammatory profiles in NP and reported a IL‐25–based endotype in CRSwNP, stratifying patients with CRSwNP into IL‐25–high (NP IL‐25‐high ) and IL‐25–low (NP IL‐25‐low ) subgroups according to the nasal IL‐25 protein level 27,46 …”

Section: Epithelium‐derived Il‐25mentioning

confidence: 99%

Role of IL‐25, IL‐33, and TSLP in triggering united airway diseases toward type 2 inflammation

Hong

Liao

Chen

et al. 2020

Allergy

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107

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Under the concept of "united airway diseases," the airway is a single organ wherein upper and lower airway diseases are commonly comorbid. The upper and lower airways are lined with respiratory epithelium that plays a vital role in immune surveillance and modulation as the first line of defense to various infective pathogens, allergens, and physical insults. Recently, there is a common hypothesis emphasizing epithelium‐derived cytokines, namely IL‐25, IL‐33, and TSLP, as key regulatory factors that link in immune‐pathogenic mechanisms of allergic rhinitis (AR), chronic rhinosinusitis (CRS), and asthma, mainly involving in type 2 inflammatory responses and linking innate and adaptive immunities. Herein, we review studies that elucidated the role of epithelium‐derived triple cytokines in both upper and lower airways with the purpose of expediting better clinical treatments and managements of AR, CRS, asthma, and other associated allergic diseases via applications of the modulators of these cytokines.

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“…Patients grouped into the high IL-25 expression cohort had higher CT sinus severity scores, higher nasal endoscopy scores, and higher downstream type-2 cytokine levels. 53 In another study, patients with high IL-25 levels were found to have nasal polyps which were more responsive to glucocorticoid therapy, 54 and this finding was corroborated in an in vitro nasal polyp explant model in which steroid exposure reduced IL-25 production. 23 …”

Section: Role Of Epithelial-derived Cytokines In Pathogenesis Of Airwmentioning

confidence: 86%

Sentinels at the wall: epithelial‐derived cytokines serve as triggers of upper airway type 2 inflammation

Patel

Kohanski

Maina

et al. 2018

Int Forum Allergy Rhinol

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Recent evidence has demonstrated an expanding role of respiratory epithelial cells in immune surveillance and modulation. Studies have been focusing on the earliest events that link epithelial injury to downstream inflammatory responses. Cytokines produced by and released from respiratory epithelial cells are among these early trigger signals. Epithelial-derived cytokines, namely thymic stromal lymphopoietin (TSLP), interleukin (IL)-25, and IL-33, have come to the forefront of recent investigations. Each of these 3 cytokines has been implicated in chronic rhinosinusitis (CRS), asthma, and atopy. Herein we review studies elucidating the roles of epithelial-derived cytokines in the pathobiology of upper airway disease, with particular emphasis on type 2 inflammatory conditions.

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Nasal IL-25 predicts the response to oral corticosteroids in chronic rhinosinusitis with nasal polyps

Cited by 25 publications

References 9 publications

Induction of IL-25 Expression in Human Nasal Polyp Epithelium by Influenza Virus Infection is Abated by Interferon-Alpha Pretreatment

Induction of IL-25 Expression in Human Nasal Polyp Epithelium by Influenza Virus Infection is Abated by Interferon-Alpha Pretreatment

Role of IL‐25, IL‐33, and TSLP in triggering united airway diseases toward type 2 inflammation

Sentinels at the wall: epithelial‐derived cytokines serve as triggers of upper airway type 2 inflammation

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