{Reference Type}: Journal Article
{Title}: Failure of the Anti-Inflammatory Parasitic Worm Product ES-62 to Provide Protection in Mouse Models of Type I Diabetes, Multiple Sclerosis, and Inflammatory Bowel Disease.
{Author}: Doonan J;Thomas D;Wong MH;Ramage HJ;Al-Riyami L;Lumb FE;Bell KS;Fairlie-Clarke KJ;Suckling CJ;Michelsen KS;Jiang HR;Cooke A;Harnett MM;Harnett W;
{Journal}: Molecules
{Volume}: 23
{Issue}: 10
{Year}: Oct 2018 17
{Factor}: 4.927
{DOI}: 10.3390/molecules23102669
{Abstract}: Parasitic helminths and their isolated secreted products show promise as novel treatments for allergic and autoimmune conditions in humans. Foremost amongst the secreted products is ES-62, a glycoprotein derived from Acanthocheilonema viteae, a filarial nematode parasite of gerbils, which is anti-inflammatory by virtue of covalently-attached phosphorylcholine (PC) moieties. ES-62 has been found to protect against disease in mouse models of rheumatoid arthritis, systemic lupus erythematosus, and airway hyper-responsiveness. Furthermore, novel PC-based synthetic small molecule analogues (SMAs) of ES-62 have recently been demonstrated to show similar anti-inflammatory properties to the parent molecule. In spite of these successes, we now show that ES-62 and its SMAs are unable to provide protection in mouse models of certain autoimmune conditions where other helminth species or their secreted products can prevent disease development, namely type I diabetes, multiple sclerosis and inflammatory bowel disease. We speculate on the reasons underlying ES-62's failures in these conditions and how the negative data generated may help us to further understand ES-62's mechanism of action.