Echinochrome A Reduces Colitis in Mice and Induces In Vitro Generation of Regulatory Immune Cells

• Published in: Marine drugs 2019-10, Vol.17 (11), p.622
• Main Authors: Oh, Su-Jeong, Seo, Yoojin, Ahn, Ji-Su, Shin, Ye Young, Yang, Ji Won, Kim, Hyoung Kyu, Han, Jin, Mishchenko, Natalia P, Fedoreyev, Sergey A, Stonik, Valentin A, Kim, Hyung-Sik
• Format: Article
• Language: English
• Subjects: Animal models; Animals; Anti-Inflammatory Agents - pharmacology; Body weight; Body weight loss; Cell differentiation; Cell growth; Cell proliferation; Cells; Colitis; Colitis - chemically induced; Colitis - drug therapy; Colon; Cytokines - metabolism; Differentiation (biology); echinochrome a; Experiments; Flow cytometry; Homeostasis; Humans; Immune system; Immunity; Immunology; Immunotherapy; Inflammation; Inflammatory bowel disease; Inflammatory bowel diseases; Inflammatory response; Intravenous administration; Lethality; Leukocytes, Mononuclear; Lymphocytes; Lymphocytes T; Macrophages; Macrophages - drug effects; marine drugs; Marine invertebrates; Mice; Naphthoquinones - pharmacokinetics; Naphthoquinones - pharmacology; Oxidative stress; Proliferation; regulatory t cells; Roles; Sea urchins; Tumor necrosis factor-TNF; Weight loss
• ISSN: 1660-3397; 1660-3397
• DOI: 10.3390/md17110622

Echinochrome A (Ech A), a natural pigment extracted from sea urchins, is the active ingredient of a marine-derived pharmaceutical called 'histochrome'. Since it exhibits several biological activities including anti-oxidative and anti-inflammatory effects, it has been applied to the management of cardiac injury and ocular degenerative disorders in Russia and its protective role has been studied for other pathologic conditions. In the present study, we sought to investigate the therapeutic potential of Ech A for inflammatory bowel disease (IBD) using a murine model of experimental colitis. We found that intravenous injection of Ech A significantly prevented body weight loss and subsequent lethality in colitis-induced mice. Interestingly, T cell proliferation was significantly inhibited upon Ech A treatment in vitro. During the helper T (Th) cell differentiation process, Ech A stimulated the generation regulatory T (Treg) cells that modulate the inflammatory response and immune homeostasis. Moreover, Ech A treatment suppressed the in vitro activation of pro-inflammatory M1 type macrophages, while inducing the production of M2 type macrophages that promote the resolution of inflammation and initiate tissue repair. Based on these results, we suggest that Ech A could provide a beneficial impact on IBD by correcting the imbalance in the intestinal immune system.