Assessment of inflammation within sporadic colorectal polyps

Background: Chronic inflammation is a risk factor for many cancers yet its relevance to sporadic colorectal cancer is often dismissed. Most cancers arise from adenomatous polyps, which are constantly exposed to physical, chemical, microbial, and hypoxic stress. We hypothesise that chronic inflammatory activity within benign precancerous polyp tissue is central to cellular transformation towards colorectal malignancy. Aims: To assess the inflammatory cell infiltrate in adenomatous polyps of varying sizes and their adjacent normal mucosa. Methods: Paraffin embedded tissue from 58 colonic polyps (29 small ⩽1 cm and 29 large >1 cm) and 35 corresponding normal mucosal biopsies from 35 patients were studied. Inflammatory cell infiltrate was assessed using immunohistochemistry. Antibodies against CD3, CD4, CD8, CD25, CD20, CD38, CD56, CD68, and neutrophil elastase were used to assess the presence of T cells (helper, cytotoxic, and activated subsets), B cells, plasma cells, NK cells, macrophages, and neutrophils, respectively. Results: In small polyps neutrophil infiltrate was increased compared to normal mucosa (p<0.001). Macrophage infiltrate was significantly increased in large polyps compared to paired normal mucosa (p<0.01). There was also a significantly increased neutrophil and activated T cell infiltrate in large polyps compared to paired normal mucosa (p<0.01 and p<0.001, respectively). Large polyps had an increased activated T cell (p<0.001) and macrophage (p<0.001) infiltrate compared to small polyps. B cells, TH cells, TC cells, mast cells, and NK cells were present in similar numbers in both normal and polyp tissue. Conclusion: Inflammatory cell infiltrates are a key feature of adenomatous polyps and manifest as acute inflammation in small polyps and acute on chronic in larger polyps. These findings may be relevant to the pathogenesis of sporadic colorectal cancer and the aetiology of this inflammatory activity warrants further investigation.