Edward J Wladis1, Kevin W Lau2, Alejandro P Adam3. 1. Ophthalmic Plastic Surgery, Department of Ophthalmology, Lions Eye Institute, Albany Medical College, Slingerlands, New York, USA. Electronic address: tedwladis@gmail.com. 2. Department of Ophthalmology, Lions Eye Institute, Albany Medical College, Slingerlands, New York, USA. 3. Department of Molecular and Cellular Physiology, Albany Medical College, Slingerlands, New York, USA.
Abstract
PURPOSE: To assess the role of nuclear factor kappa-B (NFKB) in cutaneous specimens of rosacea and unaffected tissue. METHODS: Immunohistochemical staining was performed for the activated, phosphorylated variant of NFKB (pNFKB) in eyelid specimens of rosacea (n = 12) and normal, healthy tissue (n = 12). The numbers of positively staining cells/40× microscopic field were counted across 5 consecutive fields. Additionally, quantitative Western blotting was carried out for pNFKB and NFKB in specimens of rosacea (n = 15) and normal controls (n = 14). Statistical comparisons were performed via a dedicated software package. RESULTS: The mean number of cells/40× microscopic field that stained positively for pNFKB was 18.4 (standard deviation = 15.3) for control patients and 39.3 (standard deviation = 16.9) for rosacea patients, and the difference between the 2 groups was statistically significant (P = .0024). On Western blotting, the mean ratios of pNFKB:NFKB for control and rosacea patients measured 0.58 (standard deviation = 0.81) and 3.11 (standard deviation = 3.53), respectively. The 2 groups were statistically significantly different (P = .0002). CONCLUSIONS: The activated form of NFKB is enriched in rosacea, indicating a role for this pathway in the pathogenesis of this disease. Interference with NFKB signaling may represent a novel therapy for rosacea as clinical agents become available. NOTE: Publication of this article is sponsored by the American Ophthalmological Society.
PURPOSE: To assess the role of nuclear factor kappa-B (NFKB) in cutaneous specimens of rosacea and unaffected tissue. METHODS: Immunohistochemical staining was performed for the activated, phosphorylated variant of NFKB (pNFKB) in eyelid specimens of rosacea (n = 12) and normal, healthy tissue (n = 12). The numbers of positively staining cells/40× microscopic field were counted across 5 consecutive fields. Additionally, quantitative Western blotting was carried out for pNFKB and NFKB in specimens of rosacea (n = 15) and normal controls (n = 14). Statistical comparisons were performed via a dedicated software package. RESULTS: The mean number of cells/40× microscopic field that stained positively for pNFKB was 18.4 (standard deviation = 15.3) for control patients and 39.3 (standard deviation = 16.9) for rosaceapatients, and the difference between the 2 groups was statistically significant (P = .0024). On Western blotting, the mean ratios of pNFKB:NFKB for control and rosaceapatients measured 0.58 (standard deviation = 0.81) and 3.11 (standard deviation = 3.53), respectively. The 2 groups were statistically significantly different (P = .0002). CONCLUSIONS: The activated form of NFKB is enriched in rosacea, indicating a role for this pathway in the pathogenesis of this disease. Interference with NFKB signaling may represent a novel therapy for rosacea as clinical agents become available. NOTE: Publication of this article is sponsored by the American Ophthalmological Society.