Distribution of iNOS expressions and TNF neutrophil cells as well as PGE2 and S100 Schwann cell dermal nerves in the erythema nodosum leprosum patients

ABSTRACT Background: The increase of neutrophil infiltration in the Erythema Nodusum Leprosum (ENL) is thought to have a role in releasing the free radicals and TNF? which causes dermal nerve damage. ENL occurs in leprosy patient with LL and BL type, which has lipid droplets as a synthesis site of Prostaglandin E2 that plays a role in suppressing nerve inflammation. This study investigates neutrophil distributions that express TNF? and iNOS as well as PGE2 expressions of the S100b distributions on ENL patient’s Schwann cells. Methods: This cross-sectional study used 23 samples of pedis skin biopsy from patients with MB leprosy type (10 ENL samples and 13 as control samples), from the Skin Polyclinic Sanglah Hospital, Denpasar, Indonesia. Punch biopsy of 4 mm in diameter is performed. Hematoxylin-Eosin standard staining was used to confirm the cell structure, type of leprosy, and distribution of neutrophil cells. Observation of TNF?, iNOS, PGE2, and s100b was conducted with immunohistochemistry techniques. Expression analysis was performed with immune ratio software (freeware). The PGE2, s100b, TNF?, and iNOS expression percentage were put on a list, then the T-test was performed using IBM-SPSS 21 for Windows to figure out the relationships between groups test. Results: The distributions of neutrophil were increased in the ENL group compared to the ones in the control group. The increased neutrophils appeared in the dermis area around the blood vessels. INOS and TNF? distributions on neutrophil cells increased significantly in the ENL. In line with that, the s100b expressions on the ENL were significantly lower. Conclusions: The significant increase of the iNOS and TNF? neutrophil cells in the ENL may play a role in the dermal nerve damage. This study digs into the possibility of the role of Prostaglandin E2 in maintaining the peripheral nervous system in leprosy with ENL. Hence the understanding of PGE2 as the main mediator in the inflammatory process especially in the Schwann cell damage is very important