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

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.