Volume 3 Supplement 2

9th Symposium of Experimental Rhinology and Immunology of the Nose (SERIN 2013): Abstracts

Open Access

Apoptosis factors caspases and p53 and their impact in chronic rhinosinusitis with nasal polyposis

  • Fabiana Valera1,
  • Daniel S Küpper2,
  • Rafael Malinsky2,
  • Cristiane Milanezi3,
  • João S Silva3,
  • Edwin Tamashiro2 and
  • Wilma T Anselmo-Lima2
Clinical and Translational Allergy20133(Suppl 2):O20


Published: 16 July 2013


The inflammatory process in chronic rhinosinusitis with nasal polyps (CRSwNP) has been extensively studied. However, little is known about the influence of cell death in this disease. Thus, the molecular assessment of mechanisms involved in apoptosis might shed light on the pathogenesis of CRSwNP.


To evaluate the gene expression of different apoptotic factors in patients with nasal polyps and control patients.


The mRNA expression of the apoptosis mediators caspases 3, 7, and 9, and p53 protein was analyzed using qRT-PCR in 25 nasal polyps and 18 control samples.


We observed significantly lower expression of p53 and caspases 3 and 9 genes in patients with CRSwNP compared to the controls, while caspase 7 expression was similarly expressed in both groups.


The reduced expression of these apoptosis factors in CRSwNP could be related to higher proliferation and perpetuation of inflammatory cells hindering the control of the disease. A better understanding of the possible influence of apoptosis factors on CRSwNP could be a rationale for future therapies.

Authors’ Affiliations

School of Medicine of Ribeirão Preto - University of São Paulo
ENT Division, School of Medicine of Ribeirão Preto - University of São Paulo
Biochemistry Department, School of Medicine of Ribeirão Preto - University of São Paulo


© Valera et al; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.