Commentary 10.1172/JCI134333

At last — linking ORMDL3 polymorphisms, decreased sphingolipid synthesis, and asthma susceptibility

Marsha Wills-Karp

Department of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA.

Address correspondence to: Marsha Wills-Karp, 615 North Wolfe Street, Room 7527, Baltimore, MD 21205, USA. Phone: 410.955.2452; Email: mwkarp@jhu.edu.

Find articles by Wills-Karp, M. in: JCI | PubMed | Google Scholar |

First published January 13, 2020 - More info

Published in Volume 130, Issue 2 on February 3, 2020
J Clin Invest. 2020;130(2):604–607. https://doi.org/10.1172/JCI134333.
© 2020 American Society for Clinical Investigation
First published January 13, 2020 - Version history

Asthma is a common chronic respiratory disease that has a heritable component. Polymorphisms in the endoplasmic reticular protein orosomucoid-like protein 3 (ORMDL3), which regulates sphingolipid homeostasis, have been strongly linked with childhood-onset asthma. Despite extensive investigation, a link between ORMDL3 asthma–risk genotypes and altered sphingolipid synthesis has been lacking. In this issue of the JCI, Ono et al. establish a clear association between nonallergic childhood asthma, lower whole-blood sphingolipids, and asthma-risk 17q21 genotypes. These results demonstrate that genetic variants in ORMDL3 may confer a risk of developing childhood asthma through dysregulation of sphingolipid synthesis. As such, modulation of sphingolipids may represent a promising avenue of therapeutic development for childhood asthma.

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