Low E-prostanoid 2 receptor levels and deficient induction of the IL-1β/IL-1 type I receptor/COX-2 pathway: Vicious circle in patients with aspirin-exacerbated respiratory disease

Machado-Carvalho, Liliana; Martı́n, Margarita; Torres, Rosa; Gabasa, Marta; Alobid, Isam; Mullol, Joaquim; Pujols, Laura; Roca‐Ferrer, Jordi; Picado, César

doi:10.1016/j.jaci.2015.09.028

Cited by 50 publications

(40 citation statements)

References 35 publications

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“…The IL‐1β‐induced activation of IL‐1R1 was found at the basis of pathological epileptic seizure susceptibility . The aspirin‐exacerbated respiratory disease is based on the decreased expression of IL‐1R1 and consequent decrease of the IL‐1β effects of PGE 2 induction . Increased levels of circulating sIL‐1R1 were measured in serum of patients with chronic heart disease …”

Section: Focus On the Il‐1r Familymentioning

confidence: 99%

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The family of the interleukin‐1 receptors

Boraschi

Italiani

Weil

et al. 2017

Immunological Reviews

275

225

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The extracellular forms of the IL-1 cytokines are active through binding to specific receptors on the surface of target cells. IL-1 ligands bind to the extracellular portion of their ligand-binding receptor chain. For signaling to take place, a non-binding accessory chain is recruited into a heterotrimeric complex. The intracellular approximation of the Toll-IL-1-receptor (TIR) domains of the 2 receptor chains is the event that initiates signaling. The family of IL-1 receptors (IL-1R) includes 10 structurally related members, and the distantly related soluble protein IL-18BP that acts as inhibitor of the cytokine IL-18. Over the years the receptors of the IL-1 family have been known with many different names, with significant confusion. Thus, we will use here a recently proposed unifying nomenclature. The family includes several ligand-binding chains (IL-1R1, IL-1R2, IL-1R4, IL-1R5, and IL-1R6), 2 types of accessory chains (IL-1R3, IL-1R7), molecules that act as inhibitors of signaling (IL-1R2, IL-1R8, IL-18BP), and 2 orphan receptors (IL-1R9, IL-1R10). In this review, we will examine how the receptors of the IL-1 family regulate the inflammatory and anti-inflammatory functions of the IL-1 cytokines and are, more at large, involved in modulating defensive and pathological innate immunity and inflammation. Regulation of the IL-1/IL-1R system in the brain will be also described, as an example of the peculiarities of organ-specific modulation of inflammation.

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Section: Focus On the Il‐1r Familymentioning

confidence: 99%

“…145 The aspirin-exacerbated respiratory disease is based on the decreased expression of IL-1R1 and consequent decrease of the IL-1β effects of PGE 2 induction. 146 Increased levels of circulating sIL-1R1…”

Section: Mutations Known In Diseasesmentioning

confidence: 99%

The family of the interleukin‐1 receptors

Boraschi

Italiani

Weil

et al. 2017

Immunological Reviews

275

225

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“…In particular, AERD is uniquely characterized by a dysregulation in arachidonic acid metabolism, reflecting diminished levels of the anti-inflammatory prostanoid PGE2 and increased levels of 5-lipoxygenase products LTC4, D4 and E4 17–19 . Low expression levels of the PGE2 receptor, EP2, as well as aberrant downstream receptor signaling and induction of the interleukin-1 receptor are also thought be important 20–23 . Aspirin challenges further reduce protective PGE2 and dramatically elevate leukotrienes from mast cells, eosinophils and other cells as well as PGD2 derived from mast cells 24–26 .…”

Section: Introductionmentioning

confidence: 99%

Clinical Characteristics of Patients with Chronic Rhinosinusitis with Nasal Polyps, Asthma, and Aspirin-Exacerbated Respiratory Disease

Stevens

Peters

Hirsch

et al. 2017

The Journal of Allergy and Clinical Immunology: In Practice

202

184

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Background Aspirin exacerbated respiratory disease (AERD) comprises the triad of chronic rhinosinusitis with nasal polyps (CRSwNP), asthma, and intolerance to inhibitors of the cyclooxygenase-1 (COX-1) enzyme. The prevalence of AERD remains unclear and few studies have compared the clinical characteristics of patients with AERD to those with CRSwNP alone, asthma alone, or both CRSwNP and asthma. Objective To determine the prevalence of AERD within a tertiary care setting, and to identify unique clinical features that could distinguish these patients from those with CRSwNP+Asthma or CRSwNP. Methods Electronic medical records of patients at Northwestern in Chicago, Illinois were searched by computer algorithm and then manual chart review to identify 459 patients with CRSwNP alone, 412 with CRSwNP+Asthma, 171 with AERD, and 300 with asthma only. Demographic and clinical features including sex, atopy, and sinus disease severity were characterized. Results The prevalence of AERD among CRSwNP patients was 16%. AERD patients had undergone two-fold more sinus surgeries (p<0.001) and were significantly younger at the time of their first surgery (40±13 years) than CRSwNP patients (43±14 years, p<0.05). Atopy was significantly more prevalent in patients with AERD (84%) or asthma (85%) than in CRSwNP (66%, p<0.05). More patients with AERD (13%) had corticosteroid-dependent disease than CRSwNP+Asthma (4%, p<0.01) or asthma (1%, p<0.001). Conclusions AERD is common among CRSwNP patients; even though AERD patients have CRSwNP and asthma, the clinical course of their disease is not the same as of patients who have CRSwNP and asthma but are tolerant to COX-1 inhibitors.

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“…This is also due to inhibition of coexpressed COX-1 by NSAIDs. It requires a low basal level of COX-2, whose induction defect was recently described in fibroblasts of nasal polyps from AERD patients 45. This defect is attributed to a lowered density of the interleukin-1 receptor I and a failure to induce COX-2 and membrane-associated PGE synthase (mPGES).…”

Section: Lipid Mediators In Specific Asthma Phenotypesmentioning

confidence: 99%

Eicosanoid Mediators in the Airway Inflammation of Asthmatic Patients: What is New?

Sanak

2016

Allergy Asthma Immunol Res

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Lipid mediators contribute to inflammation providing both pro-inflammatory signals and terminating the inflammatory process by activation of macrophages. Among the most significant biologically lipid mediators, these are produced by free-radical or enzymatic oxygenation of arachidonic acid named "eicosanoids". There were some novel eicosanoids identified within the last decade, and many of them are measurable in clinical samples by affordable chromatography-mass spectrometry equipment or sensitive immunoassays. In this review, we present some recent advances in understanding of the signaling by eicosanoid mediators during asthmatic airway inflammation. Eicosanoid profiling in the exhaled breath condensate, induced sputum, or their metabolites measurements in urine is complementary to the cellular phenotyping of asthmatic inflammation. Special attention is paid to aspirin-exacerbated respiratory disease, a phenotype of asthma manifested by the most profound changes in the profile of eicosanoids produced. A hallmark of this type of asthma with hypersensitivity to non-steroid anti-inflammatory drugs (NSAIDs) is to increase biosynthesis of cysteinyl leukotrienes on the systemic level. It depends on transcellular biosynthesis of leukotriene C4 by platelets that adhere to granulocytes releasing leukotriene A4. However, other abnormalities are also reported in this type of asthma as a resistance to anti-inflammatory activity of prostaglandin E2 or a robust eosinophil interferon-γ response resulting in cysteinyl leukotrienes production. A novel mechanism is also discussed in which an isoprostane structurally related to prostaglandin E2 is released into exhaled breath condensate during a provoked asthmatic attack. However, it is concluded that any single eicosanoid or even their complex profile can hardly provide a thorough explanation for the mechanism of asthmatic inflammation.

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Low E-prostanoid 2 receptor levels and deficient induction of the IL-1β/IL-1 type I receptor/COX-2 pathway: Vicious circle in patients with aspirin-exacerbated respiratory disease

Cited by 50 publications

References 35 publications

The family of the interleukin‐1 receptors

The family of the interleukin‐1 receptors

Clinical Characteristics of Patients with Chronic Rhinosinusitis with Nasal Polyps, Asthma, and Aspirin-Exacerbated Respiratory Disease

Eicosanoid Mediators in the Airway Inflammation of Asthmatic Patients: What is New?

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