| Summary: | Nasal polyposis is a common disease affecting 2-4% of the general population. The aetiology and pathogenesis are far from clear. Recent publications have suggested up-regulation of several pro-angiogenic factors including VEGF. The aim of this study was to assess and quantify the degree of angiogenesis in nasal polyposis and to determine if angiogenesis was the driving force behind polyposis. We started by developing a novel triple stain to assess remodelling in the nasal mucosa. For the first time we were able to categorically refute the common belief of angiogenesis driven polyposis. We then carried out genomic studies and identified upregulation of genes controlling the cell cycle and apoptosis, suggesting cell turnover is an important part of the pathogenesis of nasal polyps. Our gene expression data was confirmed by TUNEL staining, indicating an increased level of apoptosis in nasal polyp tissue, counterbalancing the increased cell proliferation. Inflammatory genes are also upregulated, however the data collected so far cannot distinguish between different types of inflammatory response. We carried out proteomic studies using the lu minex system but this did not clarify the situation despite using matched samples that were used in the gene array. They highlight the protein differences occurring in the polyps themselves. We have shown chemoattractants for eosinophils & macrophages (which are found in polyps), and significantly in iNOS, which is novel.
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