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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 327-335 |
| Number of pages | 9 |
| Journal | Journal of Allergy and Clinical Immunology |
| Volume | 148 |
| Issue number | 2 |
| DOIs | |
| State | Published - Aug 2021 |
Funding
C.B. was supported by grants from Flams wetenschappelijk Onderzeok ( FWO) Flanders (grant no. 1515516N , Excellence of Science [EOS] project no. GOG2318N), the Interuniversity Attraction Poles Grant P7/30, and Sanofi (grant nos. A17/TT/1942 and A19/TT/0828). B.S.B. is supported in part by a grant from the National Institute of Allergy and Infectious Diseases (grant no. U19AI136443 ). H.-U.S. is supported by grants from the Swiss National Science Foundation (grant no. 310030_184816 ). H.-U.S. also acknowledges financial support by the Russian Government Program “Recruitment of the Leading Scientists into the Russian Institutions of Higher Education.” C.B. was supported by grants from Flams wetenschappelijk Onderzeok (FWO) Flanders (grant no. 1515516N, Excellence of Science [EOS] project no. GOG2318N), the Interuniversity Attraction Poles Grant P7/30, and Sanofi (grant nos. A17/TT/1942 and A19/TT/0828). B.S.B. is supported in part by a grant from the National Institute of Allergy and Infectious Diseases (grant no. U19AI136443). H.-U.S. is supported by grants from the Swiss National Science Foundation (grant no. 310030_184816). H.-U.S. also acknowledges financial support by the Russian Government Program ?Recruitment of the Leading Scientists into the Russian Institutions of Higher Education.? Disclosure of potential conflicts of interest: B. S. Bochner has received research funding from Acerta Pharma/AstraZeneca, as well as consulting fees from Regeneron, Sanofi, and GlaxoSmithkline (GSK); receives remuneration for serving on the Scientific Advisory Board of Third Harmonic Bio and Allakos, Inc; owns stock in Allakos; is a coinventor 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; and is also a cofounder 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. Simon is a consultant for AstraZeneca, GSK, and Esocap. C. Bachert has received research funding and/or is a consultant for Sanofi, Regeneron, Genzyme, Novartis, and GSK.
Keywords
- Charcot-Leyden crystals
- Chronic rhinosinusitis
- IL-17
- activation
- biologicals
- eosinophils
- extracellular traps
- neutrophils
- type 2 inflammation
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
