European journal of molecular biology and biochemistry

EXPLORING HMGB1 PROTEIN EXPRESSION IN CHRONIC RHINOSINUSITIS WITH NASAL POLYPS: A COMPREHENSIVE IMMUNOHISTOCHEMICAL STUDY

Dr. Naveen Vasireddy

Chronic rhinosinusitis with nasal polyps (CRSwNP), HMGB1 protein, Inflammation pathogenesis, ENT pathology, Immunohistochemistry

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a multifactorial inflammatory condition of the nasal and sinus mucosa, often associated with persistent immune responses. High-mobility group box 1 (HMGB1), a nuclear protein implicated in inflammation and immune modulation, has been proposed as a key player in CRSwNP pathogenesis. This study aimed to investigate the role of HMGB1 in CRSwNP and its association with eosinophilic and non-eosinophilic inflammation. Methods: A collaborative study was conducted at Sri Lakshmi Narayana Institute of Medical Sciences, Puducherry, India, between 2018 and 2019. Forty-two nasal polyp tissue samples were collected from CRSwNP patients and compared with healthy controls. Patient diagnosis was confirmed using medical history, nasal endoscopy, computed tomography (CT) scans, and atopic status assessments. Immunohistochemical analysis was performed to evaluate HMGB1 expression alongside inflammatory markers, including IL-5, IL-8, and TNF-?. Eosinophilic infiltration was quantified using hematoxylin staining, and statistical analyses were conducted to determine correlations between inflammatory markers and clinical features. Results: HMGB1 was detected in epithelial nuclei, cytoplasm, and subepithelial regions of nasal polyp tissues. CRSwNP patients exhibited significantly higher HMGB1 expression than controls, particularly in inflammatory cells. Eosinophilic CRSwNP cases demonstrated lower HMGB1 expression in the epithelial cytoplasm and higher levels in inflammatory infiltrates compared to non-eosinophilic CRSwNP. Significant correlations were observed between HMGB1 and key inflammatory mediators, including IL-5 and TNF-?, suggesting its role in immune regulation and chronic inflammation. Conclusion: This study highlights the involvement of HMGB1 in CRSwNP pathogenesis and its potential as a biomarker for inflammatory processes in nasal polyposis. The differential expression of HMGB1 in eosinophilic and non-eosinophilic CRSwNP suggests its role in immune cell recruitment and mucosal inflammation. These findings provide new insights into CRSwNP pathophysiology and may inform future therapeutic strategies targeting HMGB1-mediated inflammation in ENT disorders. Further research is warranted to explore its potential as a therapeutic target in chronic rhinosinusitis.