Eosinophilic airway diseases: basic science, clinical manifestations and future challenges

Research output: Contribution to journalReviewResearchpeer-review

Standard

Eosinophilic airway diseases : basic science, clinical manifestations and future challenges. / Janson, Christer; Bjermer, Leif; Lehtimäki, Lauri; Kankaanranta, Hannu; Karjalainen, Jussi; Altraja, Alan; Yasinska, Valentyna; Aarli, Bernt; Rådinger, Madeleine; Hellgren, Johan; Lofdahl, Magnus; Howarth, Peter H.; Porsbjerg, Celeste.

In: European Clinical Respiratory Journal, Vol. 9, No. 1, 2040707, 2022.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Janson, C, Bjermer, L, Lehtimäki, L, Kankaanranta, H, Karjalainen, J, Altraja, A, Yasinska, V, Aarli, B, Rådinger, M, Hellgren, J, Lofdahl, M, Howarth, PH & Porsbjerg, C 2022, 'Eosinophilic airway diseases: basic science, clinical manifestations and future challenges', European Clinical Respiratory Journal, vol. 9, no. 1, 2040707. https://doi.org/10.1080/20018525.2022.2040707

APA

Janson, C., Bjermer, L., Lehtimäki, L., Kankaanranta, H., Karjalainen, J., Altraja, A., Yasinska, V., Aarli, B., Rådinger, M., Hellgren, J., Lofdahl, M., Howarth, P. H., & Porsbjerg, C. (2022). Eosinophilic airway diseases: basic science, clinical manifestations and future challenges. European Clinical Respiratory Journal, 9(1), [2040707]. https://doi.org/10.1080/20018525.2022.2040707

Vancouver

Janson C, Bjermer L, Lehtimäki L, Kankaanranta H, Karjalainen J, Altraja A et al. Eosinophilic airway diseases: basic science, clinical manifestations and future challenges. European Clinical Respiratory Journal. 2022;9(1). 2040707. https://doi.org/10.1080/20018525.2022.2040707

Author

Janson, Christer ; Bjermer, Leif ; Lehtimäki, Lauri ; Kankaanranta, Hannu ; Karjalainen, Jussi ; Altraja, Alan ; Yasinska, Valentyna ; Aarli, Bernt ; Rådinger, Madeleine ; Hellgren, Johan ; Lofdahl, Magnus ; Howarth, Peter H. ; Porsbjerg, Celeste. / Eosinophilic airway diseases : basic science, clinical manifestations and future challenges. In: European Clinical Respiratory Journal. 2022 ; Vol. 9, No. 1.

Bibtex

@article{eefcf095cf0f49f5b5b3791b48f7cd7d,
title = "Eosinophilic airway diseases: basic science, clinical manifestations and future challenges",
abstract = "Eosinophils have a broad range of functions, both homeostatic and pathological, mediated through an array of cell surface receptors and specific secretory granules that promote interactions with their microenvironment. Eosinophil development, differentiation, activation, survival and recruitment are closely regulated by a number of type 2 cytokines, including interleukin (IL)-5, the key driver of eosinophilopoiesis. Evidence shows that type 2 inflammation, driven mainly by interleukin (IL)-4, IL-5 and IL-13, plays an important role in the pathophysiology of eosinophilic airway diseases, including asthma, chronic rhinosinusitis with nasal polyps, eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome. Several biologic therapies have been developed to suppress type 2 inflammation, namely mepolizumab, reslizumab, benralizumab, dupilumab, omalizumab and tezepelumab. While these therapies have been associated with clinical benefits in a range of eosinophilic diseases, their development has highlighted several challenges and directions for future research. These include the need for further information on disease progression and identification of treatable traits, including clinical characteristics or biomarkers that will improve the prediction of treatment response. The Nordic countries have a long tradition of collaboration using patient registries and Nordic asthma registries provide unique opportunities to address these research questions. One example of such a registry is the NORdic Dataset for aSThmA Research (NORDSTAR), a longitudinal population-based dataset containing all 3.3 million individuals with asthma from four Nordic countries (Denmark, Finland, Norway and Sweden). Large-scale, real-world registry data such as those from Nordic countries may provide important information regarding the progression of eosinophilic asthma, in addition to clinical characteristics or biomarkers that could allow targeted treatment and ensure optimal patient outcomes.",
keywords = "asthma, chronic rhinosinusitis with nasal polyps, Eosinophil, eosinophilic granulomatosis with polyangiitis, hypereosinophilic syndrome, Nordic, NORDSTAR, real-world, registry, severe asthma",
author = "Christer Janson and Leif Bjermer and Lauri Lehtim{\"a}ki and Hannu Kankaanranta and Jussi Karjalainen and Alan Altraja and Valentyna Yasinska and Bernt Aarli and Madeleine R{\aa}dinger and Johan Hellgren and Magnus Lofdahl and Howarth, {Peter H.} and Celeste Porsbjerg",
note = "Publisher Copyright: {\textcopyright} 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.",
year = "2022",
doi = "10.1080/20018525.2022.2040707",
language = "English",
volume = "9",
journal = "European Clinical Respiratory Journal",
issn = "2001-8525",
publisher = "Co-Action Publishing",
number = "1",

}

RIS

TY - JOUR

T1 - Eosinophilic airway diseases

T2 - basic science, clinical manifestations and future challenges

AU - Janson, Christer

AU - Bjermer, Leif

AU - Lehtimäki, Lauri

AU - Kankaanranta, Hannu

AU - Karjalainen, Jussi

AU - Altraja, Alan

AU - Yasinska, Valentyna

AU - Aarli, Bernt

AU - Rådinger, Madeleine

AU - Hellgren, Johan

AU - Lofdahl, Magnus

AU - Howarth, Peter H.

AU - Porsbjerg, Celeste

N1 - Publisher Copyright: © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

PY - 2022

Y1 - 2022

N2 - Eosinophils have a broad range of functions, both homeostatic and pathological, mediated through an array of cell surface receptors and specific secretory granules that promote interactions with their microenvironment. Eosinophil development, differentiation, activation, survival and recruitment are closely regulated by a number of type 2 cytokines, including interleukin (IL)-5, the key driver of eosinophilopoiesis. Evidence shows that type 2 inflammation, driven mainly by interleukin (IL)-4, IL-5 and IL-13, plays an important role in the pathophysiology of eosinophilic airway diseases, including asthma, chronic rhinosinusitis with nasal polyps, eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome. Several biologic therapies have been developed to suppress type 2 inflammation, namely mepolizumab, reslizumab, benralizumab, dupilumab, omalizumab and tezepelumab. While these therapies have been associated with clinical benefits in a range of eosinophilic diseases, their development has highlighted several challenges and directions for future research. These include the need for further information on disease progression and identification of treatable traits, including clinical characteristics or biomarkers that will improve the prediction of treatment response. The Nordic countries have a long tradition of collaboration using patient registries and Nordic asthma registries provide unique opportunities to address these research questions. One example of such a registry is the NORdic Dataset for aSThmA Research (NORDSTAR), a longitudinal population-based dataset containing all 3.3 million individuals with asthma from four Nordic countries (Denmark, Finland, Norway and Sweden). Large-scale, real-world registry data such as those from Nordic countries may provide important information regarding the progression of eosinophilic asthma, in addition to clinical characteristics or biomarkers that could allow targeted treatment and ensure optimal patient outcomes.

AB - Eosinophils have a broad range of functions, both homeostatic and pathological, mediated through an array of cell surface receptors and specific secretory granules that promote interactions with their microenvironment. Eosinophil development, differentiation, activation, survival and recruitment are closely regulated by a number of type 2 cytokines, including interleukin (IL)-5, the key driver of eosinophilopoiesis. Evidence shows that type 2 inflammation, driven mainly by interleukin (IL)-4, IL-5 and IL-13, plays an important role in the pathophysiology of eosinophilic airway diseases, including asthma, chronic rhinosinusitis with nasal polyps, eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome. Several biologic therapies have been developed to suppress type 2 inflammation, namely mepolizumab, reslizumab, benralizumab, dupilumab, omalizumab and tezepelumab. While these therapies have been associated with clinical benefits in a range of eosinophilic diseases, their development has highlighted several challenges and directions for future research. These include the need for further information on disease progression and identification of treatable traits, including clinical characteristics or biomarkers that will improve the prediction of treatment response. The Nordic countries have a long tradition of collaboration using patient registries and Nordic asthma registries provide unique opportunities to address these research questions. One example of such a registry is the NORdic Dataset for aSThmA Research (NORDSTAR), a longitudinal population-based dataset containing all 3.3 million individuals with asthma from four Nordic countries (Denmark, Finland, Norway and Sweden). Large-scale, real-world registry data such as those from Nordic countries may provide important information regarding the progression of eosinophilic asthma, in addition to clinical characteristics or biomarkers that could allow targeted treatment and ensure optimal patient outcomes.

KW - asthma

KW - chronic rhinosinusitis with nasal polyps

KW - Eosinophil

KW - eosinophilic granulomatosis with polyangiitis

KW - hypereosinophilic syndrome

KW - Nordic

KW - NORDSTAR

KW - real-world

KW - registry

KW - severe asthma

U2 - 10.1080/20018525.2022.2040707

DO - 10.1080/20018525.2022.2040707

M3 - Review

C2 - 35251534

AN - SCOPUS:85126185647

VL - 9

JO - European Clinical Respiratory Journal

JF - European Clinical Respiratory Journal

SN - 2001-8525

IS - 1

M1 - 2040707

ER -

ID: 313766996