Association of interleukin-25 levels with development of aspirin induced respiratory diseases

Lee, Jong-Uk; Chang, Hun Soo; Lee, Hyeon Ju; Bae, Da-Jeong; Son, Ji-Hye; Park, Jong‐Sook; Choi, Jae Sung; Hwang, Hun Gyu; Park, Choon-Sik

doi:10.1016/j.rmed.2016.11.020

Cited by 17 publications

(18 citation statements)

References 55 publications

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“…The pathogenesis of asthma is related to Th2 cells, ILC2s, Th2 cytokines secreted by Th2 cells and ILC2s, and epithelial cell factors [ 28 ]; however, the pathogenesis of asthma has not yet been fully clarified. IL-25 is associated with bronchospasm after aspirin challenge, possibly via mechanisms other than altered LTC4 and PGD2 production [ 29 ]. Blockade of the IL-25 receptor (IL-25R) reduced many rhinovirus-induced exacerbation-specific responses, including type 2 cytokine expression, mucus production, and recruitment of eosinophils, neutrophils, basophils, and T and non-T type 2 cells [ 30 , 31 ].…”

Section: Role Of Il-25 In Asthmamentioning

confidence: 99%

Biological Properties and the Role of IL-25 in Disease Pathogenesis

Liu

Shao

Shangguan

et al. 2018

Journal of Immunology Research

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The interleukin- (IL-) 17 superfamily, a T cell-derived cytokine, consists of 6 ligands (IL-17A–IL-17F) and 5 receptors (IL-17RA–IL-17RE). IL-17A, a prototype member of this family, is involved in the pathogenesis of allergies, autoimmune diseases, allograft transplantations, and malignancies. By contrast, IL-17B is reported to be closely related to certain diseases, particularly tumors such as breast cancer, gastric cancer, and pancreatic cancer. Recently, the biological function of IL-17E (also called IL-25) in disease, particularly airway diseases, has attracted the attention of researchers. However, studies on IL-25 are scant. In this review, we detail the structural characteristics, expression patterns, responder cells, biological properties, and role of IL-25 in disease pathogenesis.

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Section: Role Of Il-25 In Asthmamentioning

confidence: 99%

Biological Properties and the Role of IL-25 in Disease Pathogenesis

Liu

Shao

Shangguan

et al. 2018

Journal of Immunology Research

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“…Furthermore, as IL-33 was found to drive the severity of Respiratory Syncytial Virus (RSV) infections in naïve mice 21 , we also investigated the effect of IL-33 in naïve versus HDM-sensitized mice upon influenza infection. And finally, we also determined the role of thymic stromal lymphopoietin (TSLP), a mediator produced by bronchial epithelial cells and that synergizes with IL-33 [22][23][24] , during virusinduced exacerbation of experimental asthma.…”

Section: Introductionmentioning

confidence: 99%

IL-33 drives influenza-induced asthma exacerbations by halting innate and adaptive antiviral immunity

Ravanetti

Dijkhuis

Dekker

et al. 2019

Journal of Allergy and Clinical Immunology

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Background. Influenza virus triggers severe exacerbations of asthma for which no adequate treatment is available. It is known that IL-33 levels correlate with exacerbation severity, but its role in the immune-pathogenesis of exacerbations has remained elusive. Objective. We hypothesized that IL-33 is necessary to drive asthma exacerbations. We intervened with the IL-33 cascade and sought to dissect its role, also in synergy with TSLP, in airway inflammation, anti-viral activity and lung function. We aimed to unveil the major source of IL-33 in the airways and IL-33-dependent mechanisms that underlie severe asthma exacerbation. Methods: Mild asthmatic patients were experimentally infected with rhinovirus. Mice were chronically exposed to house dust mite (HDM) extract and then infected with influenza to resemble key features of exacerbations in humans. Interventions included anti-IL-33-receptor ST2 and/or anti-TSLP. Results. We identified bronchial ciliated cells and Type-II alveolar cells as a major local source of IL-33 during virus-driven exacerbation in humans and mice, respectively. By blocking ST2 we demonstrated that IL-33 and not TSLP was necessary to drive exacerbations. IL-33 enhanced AHR and airway inflammation by suppressing innate and adaptive anti-viral responses and by instructing epithelial cells and dendritic cells (DCs) of HDM-sensitized mice to dampen IFN-β expression and prevent the Th1-promoting DCs phenotype. IL-33 also boosted luminal NETosis and halted cytolytic anti-viral activities, but did not affect the Th2-response. Conclusion: Interventions targeting the IL-33/ST2 axis could prove an effective acute, shortterm therapy for virus-induced asthma exacerbation.

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“…Accordingly, the levels of all of these end products are expected to be decreased after aspirin challenge or even in the basal state in NERD. However, systemic PGF245 and PGD2 levels46 and the ratio of local PGD2/PGE2 levels were increased in NERD47 compared to ATA (Fig. 6B-E).…”

Section: Differentially Methylated Cpgs Of the Genes Involved In The mentioning

confidence: 92%

“…Although systemic basal TBX2 levels were significantly higher in NERD than ATA, the levels were downregulated after aspirin challenge,48 while PGF2 and PGD2 levels were persistently elevated 4546. The different responses to aspirin challenge may be due to genetic differences in these genes between NERD and ATA.…”

Section: Differentially Methylated Cpgs Of the Genes Involved In The mentioning

confidence: 93%

Complementary Participation of Genetics and Epigenetics in Development of NSAID-exacerbated Respiratory Disease

Lee

Park

Chang

et al. 2019

Allergy Asthma Immunol Res

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Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (NERD) has attracted a great deal of attention because of its association with severe asthma. However, it remains widely underdiagnosed in asthmatics as well as the general population. Upon pharmacological inhibition of cyclooxygenase 1 by NSAIDs, production of anti-inflammatory prostaglandin E2 and lipoxins ceases, while release of proinflammatory cysteinyl leukotrienes increases. To determine the underlying mechanisms, many studies have attempted to elucidate the genetic variants, such as single nucleotide polymorphisms, responsible for alterations of prostaglandins and leukotrienes, but the results of these genetic studies could not explain the whole genetic pathogenesis of NERD. Accordingly, the field of epigenetics has been introduced as an additional contributor to genomic alteration underlying the development of NERD. Recently, changes in CpG methylation, as one of the epigenetic components, have been identified in target tissues of NERD. This review discusses in silico analyses of both genetic and epigenetic components to gain a better understanding of their complementary roles in the development of NERD. Although the molecular mechanisms underlying NERD pathogenesis remain poorly understood, genetic and epigenetic variations play significant roles. Our results enhance the understanding of the genetic and epigenetic mechanisms involved in the development of NERD and suggest new approaches toward better diagnosis and management.

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Association of interleukin-25 levels with development of aspirin induced respiratory diseases

Abstract: IL-25 is associated with bronchospasm after aspirin challenge, possibly via mechanisms other than altered LTC4 and PGD2 production.

Cited by 17 publications

References 55 publications

Biological Properties and the Role of IL-25 in Disease Pathogenesis

Biological Properties and the Role of IL-25 in Disease Pathogenesis

IL-33 drives influenza-induced asthma exacerbations by halting innate and adaptive antiviral immunity

Complementary Participation of Genetics and Epigenetics in Development of NSAID-exacerbated Respiratory Disease

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