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. 2019 Aug 10;12(4):337–347. doi: 10.21053/ceo.2019.00654

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Copyright © 2019 by Korean Society of Otorhinolaryngology-Head and Neck Surgery

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 1. — An overview of recruitment and function of neutrophils in human chronic rhinosinusitis (CRS). In response to environmental stimuli, epithelial cells secrete chemokine (C-X-C motif) ligand (CXCL) family chemokines (eg., CXCL1, CXCL2, and CXCL8) and leukotrienes to recruit neutrophils by engaging chemokine (C-X-C motif) receptor (CXCR) 1/2 and leukotriene B4 receptor (LTB4R) on neutrophils, respectively. fMetLeu-Phe (fMLP), which can be produced by colonized bacteria or damaged tissue cells, may recruit neutrophils via formyl-peptide receptor (FPR) 1/2/3. Interleukin (IL)-1 cytokine family such as IL-36γ and IL-33 participate in regulating neutrophil inflammation in CRS. IL-17A upregulates the production of full-length IL-36γ by epithelial cells. Activated IL-36γ generated by neutrophil elastase processing acts on neutrophils via IL-36R, which is upregulated by IL-6, IL-1β and Dermatophagoides pteronyssinus group (Der p) 1, and induces CXCL1, CXCL2, and CXCL8 production from neutrophils. Recruited neutrophils can kill bacteria by phagocytosis, degranulation, and formation of neutrophil extracellular traps (NETs). Activated neutrophils release extracellular vesicles. Neutrophils can also produce IL-17A, IL-36γ, IL-4/13, interferon γ (IFN-γ), oncostatin M (OSM), and transforming growth factor-β2 (TGF-β2), which may be involved in the modulation of inflammation and tissue modeling in CRS.