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. 2018 Feb;141(2):505-517.
doi: 10.1016/j.jaci.2017.09.022. Epub 2017 Oct 16.

Eosinophils and eosinophil-associated diseases: An update

Jeremy A O'Sullivan  1 , Bruce S Bochner  2
Affiliations

Eosinophils and eosinophil-associated diseases: An update

Jeremy A O'Sullivan et al. J Allergy Clin Immunol. 2018 Feb.

Abstract

The goal of this series is to offer a survey of the latest literature for clinicians and scientists alike, providing a list of important recent advances relevant to the broad field of allergy and immunology. This particular assignment was to cover the topic of eosinophils. In an attempt to highlight major ideas, themes, trends, and advances relevant to basic and clinical aspects of eosinophil biology, a search of articles published since 2015 in the Journal of Allergy and Clinical Immunology and other high-impact journals was performed. Articles were then reviewed and organized, and then key findings were summarized. Given space limitations, many outstanding articles could not be included, but the hope is that what follows provides a succinct overview of recently published work that has significantly added to our knowledge of eosinophils and eosinophil-associated diseases.

Keywords: Eosinophilopoiesis; adipose tissue; apoptosis; asthma; biologicals; chronic rhinosinusitis with nasal polyposis; eosinophil subsets; eosinophilic gastrointestinal disorder; granule biogenesis; immunoregulation.

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Figures

Fig 1
Fig 1
Recent advances in our understanding of eosinophil development, subset diversity, and functions in peripheral tissues. Bone Marrow: Eosinophils develop from GATA-1+ pre– granulocyte-macrophage progenitors (pre-GMPs) in the bone marrow. These pre-GMPs give rise to GMPs that (at least in mice) respond to IL-33 through the ST2 receptor, which promotes eosinophil development and IL-5Rα expression. GMPs express higher levels of processed XBP1 mRNA, which is essential later in development. These GMPs give rise to Siglec-F+ IL-5Rα+ mouse eosinophil precursors (EoPres). IL-33 additionally promotes eosinophil development by inducing IL-5 expression from other bone marrow cells, acting on EoPres and eosinophil lineage-committed progenitor cells (EoPs), which then follow EoPres in lineage development. EoPs express higher levels of Helios and Aiolos, members of the Ikaros family of transcription factors, which may play a role in regulating gene expression during eosinophil development and remain highly expressed in mature mouse eosinophils. Proper granule maturation requires expression of the transcription factor XBP1, the inhibition of cysteine protease activity by cystatin F, and the crystallization of the granule protein MBP-1 in a non-toxic form. Improper granule maturation can lead to the loss of cell viability and a blockade of eosinophil development. The long noncoding RNA Morrbid is highly expressed in eosinophils and other short-lived myeloid cells and has been found to prevent cell death by inhibiting the transcription of the pro-apoptotic Bcl2 family member BimActivated eosinophil: In the periphery, activation of the eosinophil leads to granule acidification, thereby priming MBP-1 by altering its conformation. Upon release, MBP-1 exerts a toxic effect on pathogens and host tissues via aggregation. Lung: Distinct eosinophil subsets exist in the mouse lung distinguishable by surface marker expression: lung-resident eosinophils (rEos) that traffic to the lung under steady-state conditions and recruited inflammatory eosinophils (iEos), which may be further subdivided by Gr-1 expression that corresponds to distinct sets of chemokine and cytokine products. rEos appear to possess regulatory properties, such as inhibiting the maturation of type 2-biased allergen-loaded DCs, that iEos do not. Sialosides on the mucins Muc4 and Muc5b bind to Siglec-F to induce eosinophil apoptosis in the mouse airway. ILC2s in the lung, in response to IL-33 signaling due to Alternaria exposure, produce IL-5 that promotes eosinophilopoiesis. Adipose Tissue: IL-5–activated mouse eosinophils indirectly promote energy expenditure in beige adipocytes by inducing the release of epinephrine and norepinephrine from alternatively activated macrophages (AAM) through IL-4 secretion. ILC2s produce IL-5 but also directly and independently act on beige adipocytes via the release of enkephalin peptides. Eosinophils directly and indirectly cause blood vessel relaxation in perivascular adipose tissue through adiponectin and catecholamine release, respectively. The catecholamines signal through β3-adrenergic receptors (β3-AR) on adipocytes to cause vessel relaxation via nitric oxide (NO) and adiponectin. Illustration by Jacqueline Schaffer.
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