Skip to main content

Advertisement

Log in

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

  • Rhinology
  • Published:
European Archives of Oto-Rhino-Laryngology Aims and scope Submit manuscript

Abstract

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-γ, 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.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2

Similar content being viewed by others

References

  1. Otto BA, Wenzel SE (2008) The role of cytokines in chronic rhinosinusitis with nasal polyps. Curr Opin Otolaryngol Head Neck Surg 16:270–274

    Article  PubMed  Google Scholar 

  2. Fokkens W, Lund V, Mullol J (2007) European position paper on rhinosinusitis and nasal polyps group. European position paper on rhinosinusitis and nasal polyps 2007. Rhinology 20:S1–S136

    Google Scholar 

  3. Cao PP, Li HB, Wang BF, Wang SB, You XJ, Cui YH, Wang DY, Desrosiers M, Liu Z (2009) Distinct immunopathologic characteristics of various types of chronic rhinosinusitis in adult Chinese. J Allergy Clin Immunol 124:478–484

    Article  PubMed  CAS  Google Scholar 

  4. Wen W, Liu W, Zhang L, Bai J, Fan Y, Xia W, Luo Q, Zheng J, Wang H, Li Z, Xia J, Jiang H, Liu Z, Shi J, Li H, Xu G (2012) Increased neutrophilia in nasal polyps reduces the response to oral corticosteroid therapy. J Allergy Clin Immunol 129:1522–1528

    Article  PubMed  CAS  Google Scholar 

  5. Wang X, Dong Z, Zhu DD, Guan B (2006) Expression profile of immune-associated genes in nasal polyps. Ann Otol Rhinol Laryngol 115:450–456

    PubMed  Google Scholar 

  6. Badolato R, Wang JM, Murphy WJ, Lloyd AR, Michiel DF, Bausserman LL, Kelvin DJ, Oppenheim JJ (1994) Serum amyloid A is a chemoattractant: induction of migration, adhesion, and tissue infiltration of monocytes and polymorphonuclear leukocytes. J Exp Med 180:203–209

    Article  PubMed  CAS  Google Scholar 

  7. Xu L, Badolato R, Murphy WJ, Longo DL, Anver M, Hale S, Oppenheim JJ, Wang JM (1995) A novel biologic function of serum amyloid A. Induction of T lymphocyte migration and adhesion. J Immunol 155:1184–1190

    PubMed  CAS  Google Scholar 

  8. Patel H, Fellowes R, Coade S, Woo P (1998) Human serum amyloid A has cytokine-like properties. Scand J Immunol 48:410–418

    Article  PubMed  CAS  Google Scholar 

  9. Lane AP, Truong-Tran QA, Myers A, Bickel C, Schleimer RP (2006) Serum amyloid A, properdin, complement 3, and toll-like receptors are expressed locally in human sinonasal tissue. Am J Rhinol 20:117–123

    PubMed  Google Scholar 

  10. Hoshino H, Laan M, Sjöstrand M, Lötvall J, Skoogh BE, Linden A (2000) Increased elastase and myeloperoxidase activity associated with neutrophil recruitment by IL-17 in airways in vivo. J Allergy Clin Immunol 105:143–149

    Article  PubMed  CAS  Google Scholar 

  11. Urieli-Shoval S, Linke RP, Matzner Y (2000) Expression and function of serum amyloid A, a major acute-phase protein, in normal and disease states. Curr Opin Hematol 7:64–69

    Article  PubMed  CAS  Google Scholar 

  12. He R, Sang H, Ye RD (2003) Serum amyloid A induces IL-8 secretion through a G protein-coupled receptor, FPRL1/LXA4R. Blood 101:1572–1581

    Article  PubMed  CAS  Google Scholar 

  13. Su SB, Gong W, Gao JL, Shen W, Murphy PM, Oppenheim JJ, Wang JM (1999) A seven-transmembrane, G protein-coupled receptor, FPRL1, mediates the chemotactic activity of serum amyloid A for human phagocytic cells. J Exp Med 189:395–402

    Article  PubMed  CAS  Google Scholar 

  14. Urieli-Shoval S, Cohen P, Eisenberg S, Matzner Y (1998) Widespread expression of serum amyloid A in histologically normal human tissues. Predominant localization to the epithelium. J Histochem Cytochem 46:1377–1384

    Article  PubMed  CAS  Google Scholar 

  15. Furlaneto CJ, Campa A (2000) A novel function of serum amyloid A: a potent stimulus for the release of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-8 by human blood neutrophil. Biochem Biophys Res Commun 268:405–408

    Article  PubMed  CAS  Google Scholar 

  16. He R, Shepard LW, Chen J, Pan ZK, Ye RD (2006) Serum amyloid A is an endogenous ligand that differentially induces IL-12 and IL-23. J Immunol 177:4072–4079

    PubMed  CAS  Google Scholar 

  17. Lane AP, Truong-Tran QA, Schleimer RP (2006) Altered expression of genes associated with innate immunity and inflammation in recalcitrant rhinosinusitis with polyps. Am J Rhinol 20:138–144

    PubMed  Google Scholar 

Download references

Acknowledgments

This study was supported by the National Natural Science Fund of China (No. U0832007, 81070771, 81070772, 81271054) and Guangdong Province Natural Science Grant (S2011010004634, S2011020002295) and a grant from the Ministry of Hygiene (No. 201202005) and Program for New Century Excellent Talents in University (No. NCET-10-0851).

Conflict of interest

No conflicts of interest to declare.

Author information

Authors and Affiliations

Authors

Corresponding authors

Correspondence to Jianbo Shi or Huabin Li.

Additional information

H.T. Wang and J. Bai have contributed equally to this study.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Wang, H., Bai, J., Ding, M. et al. Interleukin-17A contributes to the expression of serum amyloid A in chronic rhinosinusitis with nasal polyps. Eur Arch Otorhinolaryngol 270, 1867–1872 (2013). https://doi.org/10.1007/s00405-012-2295-x

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00405-012-2295-x

Keywords

Navigation