Inhibition of triggering receptor expressed on myeloid cells-1 ameliorates experimental autoimmune neuritis

Abstract

Experimental autoimmune neuritis (EAN) is a cluster of differentiation 4+ T helper 1 cell-mediated inflammatory demyelinating disease of the peripheral nervous system and serves as a useful animal model for Guillain-Barré syndrome. Triggering receptor expressed on myeloid cells-1 (TREM-1) is an important receptor involved in sepsis and the innate inflammatory response. Linear plasmid 17 (LP 17) peptide is a competitive antagonist of TREM-1. To investigate the role of TREM-1 in EAN, 64 male Lewis rats were randomly divided into four groups: Normal saline, complete Freund's adjuvant, EAN and LP 17. The present study assessed the mRNA expression levels of TREM-1, tumor necrosis factor-α and interleukin-1β in sciatic nerves and peripheral blood mononuclear cells. The results demonstrated that inhibiting TREM-1 by administering LP 17 ameliorated symptoms and reduced inflammation in EAN rats. The present study concluded that TREM-1 may be involved in the pathogenesis of EAN, and that inhibition of TREM-1 may ameliorate EAN.