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Significance Identification of the trigger of human intestinal inflammation can be a compelling clinical strategy for developing effective and target-specific antiinflammatory therapeutics. The pathomimetic “gut inflammation-on-a-chip” inspired by dextran sodium sulfate (DSS)-induced colitis models in mice enabled the independent uncoupling of complex inflammatory cross-talks and the combinatorial recoupling of individual contributing factors one at a time to identify the initiator of inflammatory responses. Our discovery suggests that an intact epithelial barrier is necessary to maintain the “homeostatic tolerance” in response to physiological host–gut microbiome cross-talks. We also expound an insight of probiotic therapy that the undamaged epithelial barrier is a prerequisite for eliciting the probiotic efficacy. Finally, the gut inflammation-on-a-chip verifies how microphysiological systems can be successfully implemented to dissect the mechanisms of gastrointestinal diseases.

Intestinal barrier dysfunction orchestrates the onset of inflammatory host–microbiome cross-talk in a human gut inflammation-on-a-chip