1. Academic Validation
  2. A novel antimicrobial peptide acting via formyl peptide receptor 2 shows therapeutic effects against rheumatoid arthritis

A novel antimicrobial peptide acting via formyl peptide receptor 2 shows therapeutic effects against rheumatoid arthritis

  • Sci Rep. 2018 Oct 2;8(1):14664. doi: 10.1038/s41598-018-32963-5.
Yoo Jung Park 1 Byunghyun Park 1 Mingyu Lee 2 Yu Sun Jeong 1 Ha Young Lee 1 Dong Hyun Sohn 3 Jason Jungsik Song 4 Joon Ha Lee 5 Jae Sam Hwang 5 Yoe-Sik Bae 6 7
Affiliations

Affiliations

  • 1 Department of Biological Sciences, Sungkyunkwan University, Suwon, 16419, Korea.
  • 2 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, 06351, Korea.
  • 3 Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan, 50612, Korea.
  • 4 Department of Internal Medicine, Division of Rheumatology, Yonsei University College of Medicine, Seoul, 03722, Korea.
  • 5 Department of Agricultural Biology, National Academy of Agricultural Science, RDA, Wanju, 55365, Korea.
  • 6 Department of Biological Sciences, Sungkyunkwan University, Suwon, 16419, Korea. yoesik@skku.edu.
  • 7 Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, 06351, Korea. yoesik@skku.edu.
Abstract

In oriental medicine, centipede Scolopendra subspinipes mutilans has long been used as a remedy for rheumatoid arthritis (RA), a well-known chronic autoimmune disorder. However, the molecular identities of its bioactive components have not yet been extensively investigated. We sought to identify bioactive molecules that control RA with a centipede. A novel antimicrobial peptide (AMP) (scolopendrasin IX) was identified from Scolopendra subspinipes mutilans. Scolopendrasin IX markedly activated mouse neutrophils, by enhancing cytosolic calcium increase, chemotactic cellular migration, and generation of superoxide anion in neutrophils. As a target receptor for scolopendrasin IX, formyl peptide receptor (FPR)2 mediates neutrophil activation induced by the AMP. Furthermore, scolopendrasin IX administration strongly blocked the clinical phenotype of RA in an autoantibody-injected model. Mechanistically, the novel AMP inhibited inflammatory cytokine synthesis from the joints and neutrophil recruitment into the joint area. Collectively, we suggest that scolopendrasin IX is a novel potential therapeutic agent for the control of RA via FPR2.

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