Over 2 million people in North America suffer from inflammatory bowel disease (IBD), a chronic and idiopathic inflammatory condition. While previous research has primarily focused on studying immune cells as a cause and therapeutic target for IBD, recent findings suggest that non-immune cells may also play a crucial role in mediating cytokine and chemokine signaling, and therefore IBD symptoms. In this study, we developed an organ-on-a-chip co-culture model of Caco2 epithelial and HUVEC endothelial cells and induced inflammation using pro-inflammatory cytokines TNF-α and IFN-γ. We tested different concentration ranges and delivery orientations (apical vs. basal) to develop a consistently inducible inflammatory response model. We then measured pro-inflammatory cytokines and chemokines IL-6, IL-8, and CXCL-10, as well as epithelial barrier integrity. Our results indicate that this model 1. induces IBD-like cytokine secretion in non-immune cells and 2. decreases barrier integrity, making it a feasible and reliable model to test the direct actions of potential anti-inflammatory therapeutics on epithelial and endothelial cells.
Copyright: © 2023 Tataru et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.