Ho SM¹, Lewis JD², Mayer EA³, Plevy SE⁴, Chuang E⁵, Rappaport SM⁶, Croitoru K⁷, Korzenik JR⁸, Krischer J⁹, Hyams JS¹⁰, Judson R¹¹, Kellis M¹², Jerrett M², Miller GW¹³, Grant ML¹⁴, Shtraizent N¹⁵, Honig G¹⁵, Hurtado-Lorenzo A¹⁵, Wu GD².Inflamm Bowel Dis. 2019 May 16;25(Supplement_2):S13-S23. doi: 10.1093/ibd/izz076.

Author information

1 University of Cincinnati, Cincinnati, Ohio.

2 Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.

3 University of California Los Angeles, Los Angeles, California.

4 Synlogic, Cambridge Massachusetts, Massachusetts.

5 Progenity, San Diego, California.

6 University of California Berkeley, Berkeley, California.

7 Mount Sinai Hospital, University of Toronto, Toronto, Canada.

8 Brigham and Women's Hospital, Boston, Massachusetts.

9 University of South Florida, Tampa, Florida.

10 Connecticut Children's Medical Center, Hartford, Connecticut.

11 United States Environmental Protection Agency, Washington, District of Columbia.

12 Massachusetts Institute of Technology, Cambridge, Massachusetts.

13 Columbia University, New York, New York.

14 Children's National Health System, Washington, District of Columbia.

15 Crohn's & Colitis Foundation, New York, New York.

Abstract

Environmental triggers is part of five focus areas of the Challenges in IBD research document, which also includes preclinical human IBD mechanisms, novel technologies, precision medicine and pragmatic clinical research. The Challenges in IBD research document provides a comprehensive overview of current gaps in inflammatory bowel diseases (IBD) research and delivers actionable approaches to address them. It is the result of a multidisciplinary input from scientists, clinicians, patients, and funders, and represents a valuable resource for patient centric research prioritization. In particular, the environmental triggers section is focused on the main research gaps in elucidating causality of environmental factors in IBD. Research gaps were identified in: 1) epidemiology of exposures; 2) identification of signatures of biological response to exposures; and 3) mechanisms of how environmental exposures drive IBD. To address these gaps, the implementation of longitudinal prospective studies to determine disease evolution and identify sub-clinical changes in response to exposures is proposed. This can help define critical windows of vulnerability and risk prediction. In addition, systems biology analysis and in silico modeling were proposed as approaches to integrate the IBD exposome for the identification of biological signatures of response to exposures, and to develop prediction models of the effects of environmental factors in driving disease activity and response to therapy. This research could lead to identification of biomarkers of exposures and new modalities for therapeutic intervention. Finally, hypothesis-driven mechanistic studies to understand gene-environment interactions and to validate causality of priority factors should be performed to determine how environment influences clinical outcomes.