Investigation into the mechanism of the blood-nerve barrier disruption in chronic inflammatory demyelinating polyradiculoneuropathy and multifocal motor neuropathy

2014 Fiscal Year Final Research Report

• Project/Area Number: 24790886
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Neurology
• Research Institution: Yamaguchi University
• Principal Investigator: SHIMIZU Fumitaka 山口大学, 医学(系)研究科(研究院), 助教 (90535254)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 自己免疫性ニューロパチー / 血液神経関門 / 慢性炎症性脱髄性根ニューロパチー / 多巣性運動ニューロパチー

Outline of Final Research Achievements

<Purpose> The aim of this project was to elucidate the severity and mechanism of breakdown of the blood-nerve barrier (BNB) in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and multifocal motor neuropathy (MMN). <Methods> We evaluated the effects of sera obtained from patients with typical CIDP/atypical CIDP/MMN and control subjects on the expression of claudin-5 and transendothelial electrical resistance (TEER) value in human peripheral nerve microvascular endothelial cells (PnMECs). <Result> Sera obtained from the patients with typical CIDP/atypical CIDP/MMN decreased the amount of claudin-5 protein levels and TEER values in PnMECs. The autocrine secretion of VEGF in PnMECs induced by MMN sera and immunoglobulin G purified from MMN sera decreased the expression of claudin-5. <Conclusion> Sera from CIDP/MMN patients disrupt the BNB function. In MMN, the autocrine secretion of VEGF in PnMECs and autoantibodies against PnMECs may be responsible for the BNB disruption.

Free Research Field

神経内科