A new study in PNAS has linked the interaction between the intestinal epithelial barrier, the gut microbiome, and immune cells to intestinal inflammation. It is thought that the gut microbiota and immune cells contribute to gut inflammation, but until now, it has been difficult to identify exactly what triggers the onset of intestinal inflammation due to the complexity of the cross-talk between the multiple different cell types.
Researchers from the Cockrell School of Engineering used their “gut inflammation-on-a-chip” microphysiological system to confirm that intestinal barrier disruption is what initiates gut inflammation. When the integrity of the cells in the epithelial barrier was compromised, subsequent exposure to immune cells and luminal microbiota caused oxidative stress and the production of inflammatory cytokines. However, when the epithelial barrier was left intact, it was able to suppress oxidative stress and cytokine production when exposed to immune cells and bacteria. Additionally, the researchers found that treating the system with probiotics reduced the oxidative stress, but did not lessen the pro-inflammatory response or repair epithelial barrier dysfunction.
Knowing how gut inflammation starts has important implications for chronic inflammatory diseases. One of the researchers, Hyun Jung Kim, was quoted in an article by GEN, saying that, “if we can determine the root cause, we can more accurately determine the most appropriate treatment.” Treatments that target the restoration of the intestinal epithelial barrier may be a compelling approach aimed at controlling local, chronic inflammation.
To read the article in PNAS, click here.
To read the University of Texas at Austin press release, click here.