APA
Click to copy
Ozkan, A., Merry, G., Chou, D. B., Posey, R. R., Stejskalová, A., Calderon, K., … Ingber, D. E. (2026). Human inflammatory bowel disease-on-a-chip for modelling disease progression, cancer initiation and sex-specific effects. Nature Biomedical Engineering.
Chicago/Turabian
Click to copy
Ozkan, Alican, G. Merry, David B. Chou, Ryan R. Posey, A. Stejskalová, K. Calderon, M. Sperry, et al. “Human Inflammatory Bowel Disease-on-a-Chip for Modelling Disease Progression, Cancer Initiation and Sex-Specific Effects.” Nature Biomedical Engineering (2026).
MLA
Click to copy
Ozkan, Alican, et al. “Human Inflammatory Bowel Disease-on-a-Chip for Modelling Disease Progression, Cancer Initiation and Sex-Specific Effects.” Nature Biomedical Engineering, 2026.
BibTeX Click to copy
@article{alican2026a,
title = {Human inflammatory bowel disease-on-a-chip for modelling disease progression, cancer initiation and sex-specific effects.},
year = {2026},
journal = {Nature Biomedical Engineering},
author = {Ozkan, Alican and Merry, G. and Chou, David B. and Posey, Ryan R. and Stejskalová, A. and Calderon, K. and Sperry, M. and Piatok, Joshua and Horváth, Viktor and Ferri, Lorenzo E. and Carlotti, Emanuela and McDonald, S. and Winton, Douglas J. and Ricciardi, R. and Bordeianou, Liliana G. and Hall, Sean R. R. and Goyal, Girija and Ingber, Donald E.}
}
Patients affected by inflammatory bowel disease (IBD) exhibit compromised intestinal barrier function and decreased mucus accumulation, as well as increased inflammation, fibrosis and cancer risk, with symptoms often being exacerbated in women during pregnancy. Here we replicate these IBD hallmarks in human-derived organ-on-a-chip devices lined by colon epithelial cells from individuals with IBD when interfaced with matched fibroblasts, cultured under flow, exposed to peristalsis-like motions and perfused with circulating immune cells. Use of heterotypic tissue recombinants revealed that IBD fibroblasts are the primary drivers of multiple IBD symptoms. In the IBD chip, inflammation and fibrosis are accentuated by peristalsis-like motions and, in female-derived chips, also by exposure to pregnancy-associated hormones. When exposed to carcinogens, the IBD chip shows increased inflammation, gene mutations and chromosome duplication, in contrast to healthy chips. These data suggest that the intestinal stroma, sex hormones and peristalsis-associated mechanical deformations have a key role in driving inflammation, fibrosis and disease progression in male and female individuals with IBD.