Increase of high mobility group box chromosomal protein 1 in eosinophilic chronic rhinosinusitis with nasal polyps

Background Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by eosinophil‐dominant infiltration in Europe and the United States. However, CRSwNP in Asia has shown different immunopathologic features. High‐mobility group protein box 1 (HMGB1) is a DNA‐binding protein that has been suggested to be involved in various chronic inflammatory diseases. The objective of this study is to investigate whether HMGB1 is augmented in the Chinese eosinophilic CRSwNP and if non‐eosinophilic CRSwNP is associated with interleukin 5 (IL‐5), IL‐8, and tumor necrosis factor α (TNF‐α). Methods Nasal polyps specimens were collected from 41 patients with CRSwNP (20 eosinophilic and 21 non‐eosinophilic) undergoing functional endoscopic sinus surgery (FESS). Biopsies of uncinate process, and ethmoidal mucosa from 9 non‐CRS patients were used as controls by means of immunohistochemistry (IHC) staining, Western blotting, and quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR). Results HMGB1‐positive expression was significantly increased in the epithelium and among the large inflammatory cells infiltration in Eos CRSwNP and non‐Eos CRSwNP as compared with controls ( p < 0.001). The HMGB1 protein and messenger RNA (mRNA) levels of HMGB1, IL‐5, IL‐8, and TNF‐α were significantly higher in eosinophilic CRSwNP than those from controls and non‐eosinophilic CRSwNP, but no significant differences in these markers were found between non‐eosinophilic CRSwNP and controls. HMGB1 expression levels correlated significantly and positively with IL‐5, IL‐8, and TNF‐α ( r s = 0.665, 0.771, and 0.724, respectively; p < 0.001) and slightly with eosinophil infiltration ( r s = 0.149; p = 0.012) and the blood eosinophils count ( r s = 0.225; p = 0.001) in all samples. Conclusion Upregulation of HMGB1 could be a significant marker typically in eosinophilic CRSwNP and it may also contribute to the pathogenesis of CRSwNP along with IL‐5, IL‐8, and TNF‐α.