4.5 Article

Interleukin-17A contributes to the expression of serum amyloid A in chronic rhinosinusitis with nasal polyps

Journal

EUROPEAN ARCHIVES OF OTO-RHINO-LARYNGOLOGY
Volume 270, Issue 6, Pages 1867-1872

Publisher

SPRINGER
DOI: 10.1007/s00405-012-2295-x

Keywords

Chronic rhinosinusitis; Nasal polyps; Serum amyloid A; Interleukin-17A; Extracellular signal-related kinase; Myeloperoxidase

Funding

  1. National Natural Science Fund of China [U0832007, 81070771, 81070772, 81271054]
  2. Guangdong Province Natural Science Grant [S2011010004634, S2011020002295]
  3. Ministry of Hygiene [201202005]
  4. Program for New Century Excellent Talents in University [NCET-10-0851]

Ask authors/readers for more resources

The expression and regulation of serum amyloid A (SAA) in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) have not been well documented. This study enrolled 24 CRSwNP patients and 19 controls to evaluate the expression of SAA in polyp tissues in Chinese adult patients and investigate underlying mechanism. The levels of SAA and interleukin (IL)-17A and myeloperoxidase (MPO) in nasal tissues were detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. In addition, the mRNA expression of SAA was examined in cultured polyp epithelial cells (PECs) in the presence of various cytokines (IFN-gamma, IL-4, IL-5 and IL-17A) using qRT-PCR, and the role of extracellular signal-related kinase (ERK) signalling in SAA expression was evaluated by western blot analysis. We found the levels of SAA, IL-17A and MPO were significantly upregulated in polyp tissues compared with the controls (p < 0.05), and significant correlations between SAA and IL-17A mRNA levels, as well as between SAA and MPO protein levels, were observed in polyp tissues (p < 0.05). In the in vitro culture system, IL-17A was found to significantly increase SAA mRNA expression in PECs via ERK signaling pathway, in a time- and dose-dependent manner (p < 0.05). Our results suggested a regulatory mechanism underlying excessive SAA production in polyp tissues, which might gain more insights into the pathophysiology of CRSwNP in Chinese adult patients.

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