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High motility group box 1 (HMGB1) protein and its receptor for advanced glycation end products (RAGE) expression in chronic rhinosinusitis without nasal polyps
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Abstract
Introduction. Chronic rhinosinusitis (CRS) affects 14% of the world population. The high motility group box 1 (HMGB1) protein triggers inflammation, cell proliferation and cell survival through its receptor for advanced glycation end products (RAGE) upon release from stressed or necrotic cells. The aim of the study was to analyze the expression and function of HMGB1 and RAGE in CRS, providing more information about HMGB1 signaling pathway in CRS, to determine its potential clinical significance.
Material and methods. Thirty-seven patients with CRS and 26 normal controls (NC) were enrolled in this study. Classification of disease severity using the SNOT-20 questionnaire, nasal endoscopy, CT scan, assessment of allergy status, microbiological and cytological analysis was performed in patients. Fresh sinus mucosa samples were obtained and analyzed by immunohistochemistry for HMGB1 and RAGE expression in epithelial cells. ELISA assay was performed to evaluate the concentration of HMGB1 in the patients’ sera.
Results. No differences were found in HMGB1 immunoexpression between CRS patients and NC, however there was a highly significant difference in RAGE immunoexpression between both groups. There was a correlation between RAGE expression and number of tissue-infiltrating lymphocytes. Further, RAGE expression positively correlated with disease severity and a positive history for allergies.
Conclusions. Interaction of HMGB1 and RAGE might be relevant to CRS pathomechanisms leading to sinus mucosa hyperproliferation. CRS pathogenesis might be especially related to the RAGE overexpression correlated with disease severity and allergy.
Abstract
Introduction. Chronic rhinosinusitis (CRS) affects 14% of the world population. The high motility group box 1 (HMGB1) protein triggers inflammation, cell proliferation and cell survival through its receptor for advanced glycation end products (RAGE) upon release from stressed or necrotic cells. The aim of the study was to analyze the expression and function of HMGB1 and RAGE in CRS, providing more information about HMGB1 signaling pathway in CRS, to determine its potential clinical significance.
Material and methods. Thirty-seven patients with CRS and 26 normal controls (NC) were enrolled in this study. Classification of disease severity using the SNOT-20 questionnaire, nasal endoscopy, CT scan, assessment of allergy status, microbiological and cytological analysis was performed in patients. Fresh sinus mucosa samples were obtained and analyzed by immunohistochemistry for HMGB1 and RAGE expression in epithelial cells. ELISA assay was performed to evaluate the concentration of HMGB1 in the patients’ sera.
Results. No differences were found in HMGB1 immunoexpression between CRS patients and NC, however there was a highly significant difference in RAGE immunoexpression between both groups. There was a correlation between RAGE expression and number of tissue-infiltrating lymphocytes. Further, RAGE expression positively correlated with disease severity and a positive history for allergies.
Conclusions. Interaction of HMGB1 and RAGE might be relevant to CRS pathomechanisms leading to sinus mucosa hyperproliferation. CRS pathogenesis might be especially related to the RAGE overexpression correlated with disease severity and allergy.
Keywords
rhinosinusitis; chronic inflammation; HMGB1; RAGE; IHC; serum
About this articleTitle
High motility group box 1 (HMGB1) protein and its receptor for advanced glycation end products (RAGE) expression in chronic rhinosinusitis without nasal polyps
Journal
Folia Histochemica et Cytobiologica
Issue
Article type
Original paper
Pages
70-78
Published online
2015-04-14
Page views
2103
Article views/downloads
1964
DOI
10.5603/FHC.a2015.0007
Pubmed
Bibliographic record
Folia Histochem Cytobiol 2015;53(1):70-78.
Keywords
rhinosinusitis
chronic inflammation
HMGB1
RAGE
IHC
serum
Authors
Karolina Dzaman
Mariola Zagor
Marta Molinska-Glura
Antoni Krzeski
