High PI3K/mTOR and low MAPK/JNK activity results in decreased apoptosis and autophagy in nasal polyposis.

INTRODUCTION

Nasal polyposis is a progressive inflammatory disease that reduces the quality of life. The role of apoptotic and autophagic pathways in nasal polyposis pathogenesis is not yet clearly known.

OBJECTIVE

In this study we aimed to investigate apoptotic (MAPK/JNK), anti-apoptotic (PI3K/mTOR) and autophagic (LC3) pathways which are related each other in the nasal polyposis tissues.

METHODS

Twenty patients with nasal polyps and fifteen patients going through an inferior turbinate reduction were included in this study. Patients with asthma, Samter triad and allergic fungal sinusitis were excluded from the study. The apoptotic and autophagic pathways were investigated in paraffin-embedded nasal tissue sections of 20 NP and 15 samples from inferior turbinate reduction by H&E and immunohistochemistry with h-score. TUNEL method with apoptotic index was used to demonstrate apoptotic cells.

RESULTS

Decreased immunoreactivity of P38 MAPK (p < 0.005) and JNK (p < 0.005) were observed in nasal polyposis compared to material from inferior turbinate reduction. This decrease may indicate a downregulation of apoptosis as demonstrated by decreased TUNEL staining in nasal polyposis (p < 0.005). The PI3K (p < 0.002) and mTOR (p < 0.005) immunoreactivities were increased in nasal polyposis. This increase indicates a downregulation of autophagy as demonstrated by decreased LC3 staining in nasal polyposis (p < 0.001).

CONCLUSION

Deficient apoptosis and autophagy through MAPK/JNK and PI3K/mTOR pathways may have a role in the pathogenesis of nasal polyposis.