S100A8 enhances IL-1β production from nasal epithelial cells in eosinophilic chronic rhinosinusitis

Ayaka Nakatani; Takeshi Tsuda; Yohei Maeda; Masaki Hayama; Daisuke Okuzaki; Sho Obata; Toshihiro Kishikawa; Kazuya Takeda; Hidenori Inohara

doi:10.1016/j.alit.2022.08.005

S100A8 enhances IL-1β production from nasal epithelial cells in eosinophilic chronic rhinosinusitis

Allergol Int. 2023 Jan;72(1):143-150. doi: 10.1016/j.alit.2022.08.005. Epub 2022 Sep 16.

Authors

Ayaka Nakatani¹, Takeshi Tsuda², Yohei Maeda³, Masaki Hayama¹, Daisuke Okuzaki⁴, Sho Obata¹, Toshihiro Kishikawa¹, Kazuya Takeda⁵, Hidenori Inohara¹

Affiliations

¹ Department of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
² Department of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka, Japan; Department of Otorhinolaryngology, Osaka National Hospital, Osaka, Japan.
³ Department of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka, Japan. Electronic address: ymaeda@ent.med.osaka-u.ac.jp.
⁴ Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
⁵ Department of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka, Japan; Department of Otolaryngology, Kindai University, Faculty of Medicine, Osaka, Japan.

PMID: 36117020
DOI: 10.1016/j.alit.2022.08.005

Abstract

Background: Chronic rhinosinusitis is classified into eosinophilic chronic rhinosinusitis (ECRS) and non-eosinophilic chronic rhinosinusitis (NECRS). ECRS is a refractory allergic disease involving a variety of immune and epithelial cells. S100A8 is a damage-associated molecular pattern that is closely related to allergic inflammation. However, the pathological implications of S100A8 in ECRS have not been clarified.

Methods: We evaluated the role of S100A8 in the pathogenesis of ECRS. Gene expression profiles of nasal polyps obtained from patients with ECRS or NECRS were evaluated using RNA sequencing.

Results: S100A8 was identified as a significantly upregulated gene in nasal polyps associated with ECRS. Immunohistochemistry consistently revealed intense S100A8 staining in nasal polyps from patients with ECRS. Human nasal epithelial cells expressed the receptor for advanced glycation end products and Toll-like receptor 4. Recombinant S100A8 protein induced interleukin-1β secretion in human nasal epithelial cells.

Conclusions: Our data demonstrate that S100A8 results in production of interleukin-1β in the nasal epithelium, which may be involved in the pathogenesis of ECRS.

Keywords: ECRS; IL-1β; Nasal polyps; S100; S100A8.

MeSH terms

Calgranulin A* / genetics
Calgranulin A* / metabolism
Chronic Disease
Cytokines / metabolism
Eosinophils
Epithelial Cells
Humans
Interleukin-1beta* / metabolism
Nasal Polyps*
Rhinitis*
Sinusitis*

Substances

Calgranulin A
Cytokines
Interleukin-1beta
S100A8 protein, human
IL1B protein, human