Autophagy is deficient in nasal polyps: implications for the pathogenesis of the disease

Nasal polyposis is characterized by persistent inflammation but the pathogenesis is complex and still debatable. Autophagy has been associated with many human health problems including chronic inflammatory airway diseases. Whether autophagy plays a role in nasal polyps and could be a therapeutic target is completely unknown.

We studied light chain 3 (LC3) protein expression, a common indication of autophagy, in fresh tissue specimens of 5 nasal polyps and 6 normal nasal mucosa by Western blot analysis. The results were also confirmed by immunohistochemistry (IHC) using additional 25 paraffin-embedded nasal tissue sections. Finally the autophagic activity was validated in nasal polyp-derived fibroblasts by evaluating the number of green fluorescent protein (GFP)-labeled LC3 puncta.

The expression of LC3 was dramatically decreased in all 5 nasal polyp tissues. In contrast, protein kinase B-mechanistic target of rapamycin (Akt-mTOR) signaling, an established negative regulator of autophagy, was significantly activated in these tissues. Immunohistochemical results further demonstrated a negative correlation between autophagy and nasal polyps (p < 0.05). GFP-LC3 puncta formation, an alternative indicator of autophagy, was also diminished in nasal polyp-derived fibroblasts (p < 0.01).

Autophagy is deficient presumably due to suppression by high Akt-mTOR activity in nasal polyps, which may provide a molecular basis for future mechanistic study of the disease.