Investigation of the presence of cannabinoid 1 receptor (CB1) andsynthesis and degradation enzymes of N-arachidonoylethanolamine (AEA) in histopathologies of psoriasis, cutaneous lupus erythematosus and lichensclerosis

The endocannabinoid system, has many functions with its enzymes, ligands and receptors. It's first discovered receptor is CB1r and the most researched ligand is N-arachidonoylethanolamine (AEA). One of the enzymes involved in the synthesis of AEA is N-acyl-phosphatidylethanolamine-hydrolyzed phospholipase D (PLD), and fatty acid amide hydrolase (FAAH) is one of the enzymes involved in its degradation. The endocannabinoid system regulates the inflammatory processes in the skin and the differentiation, apoptosis and proliferation of keratinocytes in the epidermis. Because of these functions this system is a potential target in inflammatory skin diseases with hyperkeratosis. So we aimed to investigate the effect of the endocannabinoid system in psoriasis, cutaneous lupus erythematosus (CLE) and lichen sclerosis (LS) and compare the synthesis and degradation enzymes of AEA, phospholipase D and FAAH, and CB1r with healthy skin. A prospective, simple randomized, observational study with control group was made. CB1r, FAAH and PLD reactivity and localization in the epidermis were analyzed immunohistochemically and compared with the control group. TNF-α levels as an inflammation marker were measured by ELISA. Immunoreactivity and distribution of CB1r, FAAH ve PLD were different in disease and control groups. In this study, for the first time it is shown that that the loss of CB1r has an effect on the elongation of the rete ridges, which is a typical finding of psoriasis, and in the pathophysiology of CLE and LS, endocannabinoid system defect is present.