Immunohistochemical Analysis of Differences of Toll-Like Receptor 2, Mast Cells, and Neurofilaments between Granulomatous Rosacea and Non-Granulomatous Rosacea

Background: Granulomatous rosacea is a distinct variant of rosacea because of its unique histopatholiogic findings. However, the pathogenesis of granulomatous rosacea has not yet been clearly demonstrated. Aims and Objectives: The aim of this study was to investigate the expression of toll-like receptor 2, mast cells, and neurofilaments in the granulomatous rosacea compared with the non-granulomatous rosacea. Materials and Methods: Biopsy specimens were obtained from 12 patients with erythematotelangiectatic rosacea, 11 patients with granulomatous rosacea, and 11 control patients. Biopsy tissue blocks were subjected to immunohistochemical staining using antibodies against toll-like receptor 2, mast cells, and neurofilaments. Results: In granulomatous rosacea, the expression of mast cells increased significantly, compared to the erythematotelangiectatic rosacea and the control group (P-value = 0.001 and 0.013, respectively). Additionally, the expression of toll-like receptor 2 in the granulomatous rosacea group was higher than that in the control group (P-value = 0.04). Conclusion: The results of this study suggest that the increased expression of mast cells may be a sign of chronic, later stage of granulomatous rosacea compared to the erythematotelangiectatic rosacea. The increased expression of toll-like receptor 2 suggests that cathelicidin-induced neuroimmune pathogenesis also contributes to the pathophysiology of granulomatous rosacea.

Automated summary

The study found a significant increase in the expression of mast cells in granulomatous rosacea, and higher expression of toll-like receptor 2 compared to the control group. These results suggest that the increased expression of mast cells may indicate a chronic, later stage of granulomatous rosacea, while the increase in toll-like receptor 2 expression implies that cathelicidin-induced neuroimmune pathogenesis also contributes to the pathophysiology of granulomatous rosacea.