Potential Role of Interleukin-25/Interleukin-33/Thymic Stromal Lymphopoietin-Fibrocyte Axis in the Pathogenesis of Allergic Airway Diseases

Yao, Xiujuan; Liu, Xiaofang; Wang, Xiangdong

doi:10.4103/0366-6999.238150

Cited by 11 publications

(10 citation statements)

References 40 publications

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“…Further studies discovered that a wide range of tissues and cells can produce and secrete IL‐25, including airway and intestinal epithelial cells, endothelial cells, liver cells, kidney cells, activated Th2 cells, eosinophils, basophils, alveolar macrophages (after stimulated by inhaled antigens), bone marrow–derived mast cells, and fibroblasts 10 . With research advancing, the latest study disclosed a rare epithelial cell type, the tuft cell, to be the sole source of IL‐25 in the small intestine 35,36 .…”

Section: Epithelium‐derived Il‐25mentioning

confidence: 99%

“…Allergen exposure ultimately evokes mast cell activation and degranulation, eosinophil recruitment and infiltration, type 2 (eg, T‐helper cells) cell activation and polarization, and antigen‐specific immunoglobulin E (IgE) production. Meanwhile, type 2 cytokine response bias characterized by an over‐production of interleukin (IL)‐4 (a cytokine that causes isotype class switching in B cells to produce IgE), IL‐5 (a cytokine that promotes eosinophil activation and recruitment), and IL‐13 (a cytokine that triggers mucus hypersecretion and airway hypersensitivity) can be observed in both upper and lower airways 9‐19 . Nasal allergen exposure tests in nonasthmatic AR patients result in eosinophilia in both upper and lower airway mucosa as well as peripheral blood 20,21 .…”

Section: Introductionmentioning

confidence: 99%

“…With Toll‐like receptors (TLR) and nucleotide‐binding oligomerization domain (NOD)–like receptors (NLR) expressed on the surface, epithelial cells can recognize structurally conservative pathogen‐associated molecular patterns (PAMPs) in pathogens and respond to these exogenous danger signals by eliciting immune responses. The important response of the epithelium to the PAMP‐TLR/NLR interaction is the secretion of various cytokines, especially IL‐25, IL‐33, and TSLP, which can induce both innate and adaptive immune responses and lean inflammations toward a type 2 immune response bias 10,32 …”

Section: Introductionmentioning

confidence: 99%

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

Hong

Liao

Chen

et al. 2020

Allergy

159

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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Section: Epithelium‐derived Il‐25mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Hong

Liao

Chen

et al. 2020

Allergy

159

107

View full text Add to dashboard Cite

show abstract

“…In contrast, inhibition of the EMT process may slow airway remodeling in asthma ( 39 ). The increased expression of IL-33 in airway epithelial cells is closely related to the severity of asthma ( 40 ), and IL-33 has been shown to not only exacerbate airway inflammation ( 41 ) but also promote airway remodeling in asthma ( 42 – 44 ). Downstream signaling molecules of ST2, including MyD88, NF-κB p65, and MAPK, are then activated.…”

Section: Discussionmentioning

confidence: 99%

Epithelial-Mesenchymal Transition in Asthma Airway Remodeling Is Regulated by the IL-33/CD146 Axis

Sun

et al. 2020

Front. Immunol.

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Epithelial-mesenchymal transition (EMT) is essential in asthma airway remodeling. IL-33 from epithelial cells is involved in pulmonary fibrosis. CD146 has been extensively explored in cancer-associated EMT. Whether IL-33 regulates CD146 in the EMT process associated with asthma airway remodeling is still largely unknown. We hypothesized that EMT in airway remodeling was regulated by the IL-33/CD146 axis. House dust mite (HDM) extract increased the expression of IL-33 and CD146 in epithelial cells. Increased expression of CD146 in HDM-treated epithelial cells could be blocked with an ST2-neutralizing antibody. Moreover, HDM-induced EMT was dependent on the CD146 and TGF-β/SMAD-3 signaling pathways. IL-33 deficiency decreased CD146 expression and alleviated asthma severity. Similarly, CD146 deficiency mitigated EMT and airway remodeling in a murine model of chronic allergic airway inflammation. Furthermore, CD146 expression was significantly elevated in asthma patients. We concluded that IL-33 from HDM extract-treated alveolar epithelial cells stimulated CD146 expression, promoting EMT in airway remodeling in chronic allergic inflammation.

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“…Important original studies and reviews about the role of IL-25/IL-33/TSLP in AADs are listed here. 11–18…”

Section: Il-25 Il-33 and Tslp In Allergic Airway Diseasesmentioning

confidence: 99%

IL-25/IL-33/TSLP contributes to idiopathic pulmonary fibrosis: Do alveolar epithelial cells and (myo)fibroblasts matter?

Zhang

Dai

2020

Exp Biol Med (Maywood)

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Idiopathic pulmonary fibrosis is a relentless fibrotic disease with largely unknown etiologies. Currently, the crosstalk between alveolar epithelial cells and lung-resident mesenchymal cells (especially [myo]fibroblasts) is considered to be the central pathogenesis to initiate and propagate the fibrotic process. Unfortunately, the master switch hidden in the profibrotic milieu that mediates pathogenic epithelial-mesenchymal interactions is still not well elucidated. Thus, the definite treatment target that can block and cure idiopathic pulmonary fibrosis is now lacking. Based on the previous studies, we proposed the notion that epithelium-derived triple type 2 cytokines, i.e. interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP) are important pro-fibrotic mediators in idiopathic pulmonary fibrosis via two possible mechanisms: (1) paracrine pathway: directly acting on (myo)fibroblast. There may exist a structural and functional axis of (IL-25/IL-33/TSLP)+alveolar epithelial cells-(IL-25R/IL-33R/TSLPR)+ (myo)fibroblasts in fibroblastic foci of idiopathic pulmonary fibrosis patients. The crosstalk between alveolar epithelium and the adjacent mesenchymal compartment is well established by the binding of IL-25/IL-33/TSLP expressed on alveolar epithelial cells with their corresponding receptors (i.e. IL-17BR/sT2L/TSLPR) expressed on (myo)fibroblasts; (2) autocrine pathway: directly acting on alveolar epithelial cells. Alveolar epithelial cells may act as both cellular sources and targets of IL-25/IL-33/TSLP. Autocrine IL-25/IL-33/TSLP causes salient injury and phenotypic changes of alveolar epithelial cells. Thus, epithelium-derived IL-25/IL-33/TSLP may be the novel promising treatment target for the cure of idiopathic pulmonary fibrosis. Impact statement We suggest a novel modality in terms of IL-25/IL-33/TSLP’s pro-fibrotic role in IPF. First, IL-25/IL-33/TSLP fully activates (myo)fibroblasts in fibroblastic foci (FF) in a paracrine-dependent manner. (IL-25/IL-33/TSLP)+alveolar epithelial cells-(IL-25R/IL-33R/TSLPR)+ (myo)fibroblasts axis may contribute greatly to the abnormal epithelial-mesenchymal crosstalk and lung fibrosis. Second, IL-25/IL-33/TSLP causes significant injury and phenotypic changes of alveolar epithelial cells in an autocrine-dependent manner. By acting directly on the two most important cells in the fibrotic process, i.e. alveolar epithelial cells and (myo)fibroblasts, we support the notion that biological therapies targeting IL-25/IL-33/TSLP will shed new light on the cure of IPF patients.

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Potential Role of Interleukin-25/Interleukin-33/Thymic Stromal Lymphopoietin-Fibrocyte Axis in the Pathogenesis of Allergic Airway Diseases

Cited by 11 publications

References 40 publications

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

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

Epithelial-Mesenchymal Transition in Asthma Airway Remodeling Is Regulated by the IL-33/CD146 Axis

IL-25/IL-33/TSLP contributes to idiopathic pulmonary fibrosis: Do alveolar epithelial cells and (myo)fibroblasts matter?

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