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Review
. 2021 Aug;148(2):327-335.
doi: 10.1016/j.jaci.2021.03.024. Epub 2021 Apr 21.

Rethinking neutrophils and eosinophils in chronic rhinosinusitis

Tim Delemarre  1 , Bruce S Bochner  2 , Hans-Uwe Simon  3 , Claus Bachert  4
Affiliations
Review

Rethinking neutrophils and eosinophils in chronic rhinosinusitis

Tim Delemarre et al. J Allergy Clin Immunol. 2021 Aug.

Abstract

Chronic rhinosinusitis (CRS) often is characterized by an eosinophilic inflammatory pattern, nowadays referred to as type 2 inflammation, although the mucosal inflammation is dominated by neutrophils in about a third of the patients. Neutrophils are typically predominant in 50% of patients with CRS without nasal polyps, but also are found to play a role in patients with severe type 2 CRS with nasal polyp disease. This review aims at summarizing the current understanding of the eosinophilic and neutrophilic inflammation in CRS pathophysiology, and provides a discussion of their reciprocal interactions and the clinical impact of the mixed presentation in patients with severe type 2 CRS with nasal polyps. A solid understanding of these interactions is of utmost importance when treating uncontrolled severe CRS with nasal polyps with biologicals that are preferentially directed toward type 2 inflammation. We here focus on recent findings on both eosinophilic and neutrophilic granulocytes, their subgroups and the activation status, and their interactions in CRS.

Keywords: Charcot-Leyden crystals; Chronic rhinosinusitis; IL-17; activation; biologicals; eosinophils; extracellular traps; neutrophils; type 2 inflammation.

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Conflict of interest statement

Disclosure of potential conflicts of interest: C.B. is has received research funding and/or is a consultant for Sanofi, Regeneron, Genzyme, Novartis, and GSK. T.D. declares that he has no relevant conflicts of interest. B.S.B. has received research funding from Acerta Pharma / AstraZeneca, as well as consulting fees from Regeneron, Sanofi, and GlaxoSmithkline. B.S.B. also receives remuneration for serving on the scientific advisory board of Third Harmonic Bio and Allakos, Inc. and owns stock in Allakos. He is a co-inventor on existing Siglec-8–related patents and thus may be entitled to a share of royalties received by Johns Hopkins University during development and potential sales of such products. B.S.B. is also a co-founder of Allakos; the terms of this arrangement are being managed by Johns Hopkins University and Northwestern University in accordance with their conflict of interest policies. H.U.S. is a consultant for AstraZeneca, GlaxoSmithKline, and Esocap.

Figures

Figure 1:
Figure 1:
Mixed presence of eosinophils and neutrophils in CRSwNP. Eosinophils (left) and neutrophils (right) in the mucosa of CRSwNP via immunohistochemistry staining of major basic protein (MBP) and elastase, respectively.
Figure 2:
Figure 2:
Pathophysiology of a mixed eosinophilic-neutrophilic inflammation in severe type 2 CRSwNP. Both an eosinophilic inflammation (left side) and a neutrophilic inflammation (right side) contribute to the pathophysiology in the mucosa of severe type 2 CRSwNP. Both responses impact the course of the disease and reciprocal interactions between eosinophils and neutrophils contribute to the persistency and severity of the disease. EETs, eosinophil extracellular traps; NETs, neutrophil extracellular traps; CLCs, Charcot-Leyden crystals, MBP, major basic protein; ECP, eosinophil cationic protein; EDN, eosinophil-derived neurotoxin; TSLP, thymic stromal lymphopoietin; RANTES, regulated on activation, normal cell expressed and secreted.
See this image and copyright information in PMC

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