Lichen planus (LP) is an inflammatory disease of the skin and mucous membranes. Autoimmunity has been suggested as a possible cause of this disease. The cyclooxygenase enzymes (COX-1, COX-2) are the key enzymes in the conversion of arachidonic acid into prostaglandins. Prostaglandin E2 (PGE2), a key product of COX-2, has an immunomodulatory role.Aim.
To map levels of COX-2 and PGE2 in cutaneous LP lesions and evaluate their role in the pathogenesis of the disease.Methods.
In total, 31 patients with classic cutaneous LP and 30 age- and sex-matched healthy controls were enrolled. Skin biopsies were taken from the lesional and nonlesional skin of patients, and from the normal skin of controls. COX-2 mRNA expression was detected by real-time reverse transcription quantitative PCR, and PGE2 was detected by ELISA in skin biopsies from patients and controls.Results.
Our analysis revealed a significantly higher expression of COX-2 mRNA and PGE2 in the LP skin biopsies compared with the control biopsies (P < 0.001 and P < 0.001, respectively). Lesional biopsies showed significantly higher expression of COX-2 mRNA and PGE2 compared with nonlesional biopsies. The levels of COX-2 and PGE2 were not found to be correlated with age, sex or disease duration.Conclusions.
COX-2 and its product PGE2 are strongly expressed in LP skin lesions, indicating that they have a role in the pathogenesis of LP through their immunomodulatory effects.