Wednesday, 13 May 2020 21:49

MIT: Physiom-on-a-Chip model developed Featured

Bioengineers from the laboratory of the Massachusetts Institute of Technology in Cambridge,  have developed a multi-tissue model to study the relationships between organs and the immune system.

The new system combines three microphysiological systems: one simulates a chronic inflammatory bowel disease (ulcerative colitis), a second is a miniaturized, healthy liver tissue and the third represents the immune system. Together, they simulate the intestinal-liver-immune axis. With their model, they were able to study the progression of ulcerative colitis (UC) outside of the body.

Using the triple combination, the researchers led by Prof. Linda Griffith observed, that the chronic inflammation of the intestinal tissue decreased through the healthy liver tissue. They also found increased activity of gene expressions and pathway activations for certain metabolic processes and immune reactions.

Through the addition of circulating Th17- and CD4+ T-Reg cells, the inflammation was enhanced and enabled the modeling of autoimmune liver disease. TH17 cells are a special type of T-helper cells that are associated with the development of chronic inflammation and autoimmune diseases. The CD4-positive T-helper cells are regulatory T-cells (Tregs). They act as a brake on immune reactions.

The researchers consider their model to be a way to influence the complexity of replicated disease models under controlled and systematic conditions. The model could help to clarify the paradoxical role of circulating immune cells and the microbiome in chronic inflammatory diseases.

Original publication:
Martin Trapecar, Catherine Communal, Jason Velazquez, Christian Alexander Maass, Yu-Ja Huang, Kirsten Schneider, Charles W. Wright, George Eng, Omer Yilmaz, David Trumper, Linda G. Griffith (2020). Gut-Liver physiomimetics reveal paradoxical modulation of IBD-related inflammation by short-chain fatty acids. Cell Syst. 10(3): 223-239.e9. doi: 10.1016/j.cels.2020.02.008.