5‐/12‐Lipoxygenase‐linked cascade contributes to the <scp>IL</scp>‐33‐induced synthesis of <scp>IL</scp>‐13 in mast cells, thus promoting asthma development

Ro, MyungJa; Lee, A-Jin; Kim, Jae Hong

doi:10.1111/all.13294

Cited by 30 publications

(26 citation statements)

References 37 publications

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“…Ro et al proposed a “MyD88‐5‐/12‐LO‐BLT2‐NF‐κB” cascade contributing to the asthmatic development and exacerbation via IL‐33–induced IL‐13 production from mast cells 74 . A following study claimed that LTB4‐BLT1 axis in nonimmune cells, most likely lung epithelial cells, functioned as an upstream controller of IL‐33 production, leading to ILC2 activation and a subsequent allergic Th2 response 75 .…”

Section: Epithelium‐derived Il‐33mentioning

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

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‐33mentioning

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

159

107

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“…The association atopy‐NERD is inconsistent; however, up to 60% of NIUA patients showed specific IgE to Dermatophagoides pteronyssinus , which apparently influences ASA tolerance development . The innate immune system could participate in NSAIDs hypersensitivity through cytokines such as IL‐33 and thymic stromal lymphopoietin, orchestrating eosinophilic inflammation, mast cell activation and IgE synthesis …”

Section: Underlying Mechanisms and Endotypesmentioning

confidence: 99%

Progress in understanding hypersensitivity reactions to nonsteroidal anti‐inflammatory drugs

Doña

Pérez‐Sánchez

Eguiluz‐Gracia

et al. 2019

Allergy

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Nonsteroidal anti‐inflammatory drugs (NSAIDs), the medications most commonly used for treating pain and inflammation, are the main triggers of drug hypersensitivity reactions. The latest classification of NSAIDs hypersensitivity by the European Academy of Allergy and Clinical Immunology (EAACI) differentiates between cross‐hypersensitivity reactions (CRs), associated with COX‐1 inhibition, and selective reactions, associated with immunological mechanisms. Three phenotypes fill into the first group: NSAIDs‐exacerbated respiratory disease, NSAIDs‐exacerbated cutaneous disease and NSAIDs‐induced urticaria/angioedema. Two phenotypes fill into the second one: single‐NSAID‐induced urticaria/angioedema/anaphylaxis and single‐NSAID‐induced delayed reactions. Diagnosis of NSAIDs hypersensitivity is hampered by different factors, including the lack of validated in vitro biomarkers and the uselessness of skin tests. The advances achieved over recent years recommend a re‐evaluation of the EAACI classification, as it does not consider other phenotypes such as blended reactions (coexistence of cutaneous and respiratory symptoms) or food‐dependent NSAID‐induced anaphylaxis. In addition, it does not regard the natural evolution of phenotypes and their potential interconversion, the development of tolerance over time or the role of atopy. Here, we address these topics. A state of the art on the underlying mechanisms and on the approaches for biomarkers discovery is also provided, including genetic studies and available information on transcriptomics and metabolomics.

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“…5 Furthermore, LTB 4 receptors, BLT1 and BLT2, were suggested to contribute to the development of asthmatic airway inflammation. 6,7 In the present study, we examined whether BLT1/2-cascade plays a role in the development of neutrophil-dominant airway inflammation.…”

Section: Leukotriene B 4 Receptors Mediate the Production Of Il-17 Tmentioning

confidence: 99%

Leukotriene B₄ receptors mediate the production of IL‐17, thus contributing to neutrophil‐dominant asthmatic airway inflammation

Kwon

Kim

2019

Allergy

Self Cite

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5‐/12‐Lipoxygenase‐linked cascade contributes to the IL‐33‐induced synthesis of IL‐13 in mast cells, thus promoting asthma development

Abstract: Our results suggest that "MyD88-5-/12-LO-BLT2-NF-κB" cascade significantly contributes to the IL-33-induced synthesis of IL-13 in mast cells, thus potentially contributing to asthmatic development and exacerbation.

Cited by 30 publications

References 37 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

Progress in understanding hypersensitivity reactions to nonsteroidal anti‐inflammatory drugs

Leukotriene B₄ receptors mediate the production of IL‐17, thus contributing to neutrophil‐dominant asthmatic airway inflammation

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5‐/12‐Lipoxygenase‐linked cascade contributes to the IL‐33‐induced synthesis of IL‐13 in mast cells, thus promoting asthma development

Abstract: Our results suggest that "MyD88-5-/12-LO-BLT2-NF-κB" cascade significantly contributes to the IL-33-induced synthesis of IL-13 in mast cells, thus potentially contributing to asthmatic development and exacerbation.

Cited by 30 publications

References 37 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

Progress in understanding hypersensitivity reactions to nonsteroidal anti‐inflammatory drugs

Leukotriene B4 receptors mediate the production of IL‐17, thus contributing to neutrophil‐dominant asthmatic airway inflammation

Contact Info

Product

Resources

About

Leukotriene B₄ receptors mediate the production of IL‐17, thus contributing to neutrophil‐dominant asthmatic airway inflammation