Modulation of kallikrein-kinin system by the angiotensin-converting enzyme inhibitor alleviates experimental autoimmune encephalomyelitis.

The objectives of this study were to determine whether bradykinin is involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of MS, and whether bradykinin control by the ACE inhibitor could be a therapeutic target in MS. The ACE inhibitor enalapril (1.0 or 0.2 mg/kg/day) was orally administered to EAE mice and the serum levels of bradykinin and cytokines in EAE mice were analyzed. As a result, the administration of enalapril increased serum bradykinin levels, decreased the clinical and pathological severity of EAE, and attenuated interleukin-17-positive cell invasion into CNS. Additionally, bradykinin receptor antagonist administration reduced the favorable effects of enalapril. Our results suggest that bradykinin is involved in the pathomechanism underlying CNS inflammation in EAE, possibly through inhibiting cell migration into CNS. Control of the kallikrein/kinin system using ACE inhibitors could be a potential therapeutic strategy in MS. PMID: 24996009 [PubMed - as supplied by publisher]
Source: Clinical and Developmental Immunology - Category: Allergy & Immunology Authors: Tags: Clin Exp Immunol Source Type: research