Late Breaking Abstract - Anti-IL-5 mepolizumab minimally influences residual blood eosinophils in severe asthma

Hulst, Glenn Van; Jorssen, Joseph; Jacobs, Nathalie; Henket, Monique; Louis, Renaud; Schleich, Florence; Bureau, Fabrice; Desmet, Christophe

doi:10.1183/13993003.congress-2021.pa890

Cited by 3 publications

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GPR43 in eosinophils prevents the emergence of pathogenic Siglec-F^hineutrophils in allergic airway inflammation

Yu,

Kim,

Song

et al. 2024

Preprint

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Eosinophils are major effector cells in type 2 immune responses, contributing to host defense and allergic diseases. They also play critical roles in maintaining tissue homeostasis by regulating various immune cell types. However, evidence of the crosstalk between eosinophils and neutrophils is limited. Here, we show that eosinophils directly associate with neutrophils in the lungs of asthma-induced mice. Eosinophil-specific deficiency of the short-chain fatty acid receptor GPR43 results in hyperactivation of eosinophils and increases the expression of neutrophil chemoattractants and PECAM-1, thus enhancing the interaction between eosinophils and neutrophils. This binding event exposes the neutrophils to eosinophil-derived IL-4 and GM-CSF, which induces the conversion of conventional neutrophils into more pathogenic Siglec-Fhineutrophils that strongly enhance Th17 cell differentiation and aggravate asthma symptoms. These results reveal GPR43 as a critical regulator of eosinophils and highlight that eosinophils have a hitherto little-known ability to directly modulate neutrophil differentiation and function.One Sentence SummaryEosinophils directly recruit neutrophils and induce their differentiation into a pathogenic Siglec-Fhisubset in allergic airway inflammation.

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GPR43 in eosinophils prevents the emergence of pathogenic Siglec-F^hineutrophils in allergic airway inflammation

Yu,

Kim,

Song

et al. 2024

Preprint

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Eosinophils, beyond IL-5

Esnault

Johansson

Mathur

2021

Cells

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Eosinophils as Drivers of Severe Eosinophilic Asthma: Endotypes or Plasticity?

Hulst

Bureau

2021

IJMS

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Asthma is now recognized as a heterogeneous disease, encompassing different phenotypes driven by distinct pathophysiological mechanisms called endotypes. Common phenotypes of asthma, referred to as eosinophilic asthma, are characterized by the presence of eosinophilia. Eosinophils are usually considered invariant, terminally differentiated effector cells and have become a primary therapeutic target in severe eosinophilic asthma (SEA) and other eosinophil-associated diseases (EADs). Biological treatments that target eosinophils reveal an unexpectedly complex role of eosinophils in asthma, including in SEA, suggesting that “not all eosinophils are equal”. In this review, we address our current understanding of the role of eosinophils in asthma with regard to asthma phenotypes and endotypes. We further address the possibility that different SEA phenotypes may involve differences in eosinophil biology. We discuss how these differences could arise through eosinophil “endotyping”, viz. adaptations of eosinophil function imprinted during their development, or through tissue-induced plasticity, viz. local adaptations of eosinophil function through interaction with their lung tissue niches. In doing so, we also discuss opportunities, technical challenges, and open questions that, if addressed, might provide considerable benefits in guiding the choice of the most efficient precision therapies of SEA and, by extension, other EADs.

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Late Breaking Abstract - Anti-IL-5 mepolizumab minimally influences residual blood eosinophils in severe asthma

Cited by 3 publications

References 0 publications

GPR43 in eosinophils prevents the emergence of pathogenic Siglec-F^hineutrophils in allergic airway inflammation

GPR43 in eosinophils prevents the emergence of pathogenic Siglec-F^hineutrophils in allergic airway inflammation

Eosinophils, beyond IL-5

Eosinophils as Drivers of Severe Eosinophilic Asthma: Endotypes or Plasticity?

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Late Breaking Abstract - Anti-IL-5 mepolizumab minimally influences residual blood eosinophils in severe asthma

Cited by 3 publications

References 0 publications

GPR43 in eosinophils prevents the emergence of pathogenic Siglec-Fhineutrophils in allergic airway inflammation

GPR43 in eosinophils prevents the emergence of pathogenic Siglec-Fhineutrophils in allergic airway inflammation

Eosinophils, beyond IL-5

Eosinophils as Drivers of Severe Eosinophilic Asthma: Endotypes or Plasticity?

Contact Info

Product

Resources

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GPR43 in eosinophils prevents the emergence of pathogenic Siglec-F^hineutrophils in allergic airway inflammation

GPR43 in eosinophils prevents the emergence of pathogenic Siglec-F^hineutrophils in allergic airway inflammation