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<h1 style="color: #000 !important;">Abstract 20150421</h1>
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<p><strong><의공학연구소 정례세미나></strong></p><p><strong>연자 : 김현중 박사 (University of Texas at Austin)</strong></p><p><strong>주제 : </strong><strong>Microengineered
Human Gut-on-a-Chip for Dissecting Intestinal </strong></p><p><strong> Inflammatory Disease</strong></p><p><strong>일시 : 4월 21일 화요일 17:00~</strong></p><p><strong>장소 : 아산생명과학연구원 교육연구관 4층 회의실 </strong></p><p><strong>Abstract:</strong></p><p>Human
intestinal inflammatory diseases involve debilitating inflammation and mucosal
injury caused by complex interactions between gut microbes, intestinal epithelial
cells, immune system, and peristalsis-associated mechanical deformations.
However, it has not been possible to precisely define how these interacting
factors contribute to the disease development or to responses to clinical
therapies because human-relevant experimental models that can independently and
collectively control these factors do not exist. Here, we describe a
microengineered human ‘Gut-on-a-Chip’ microsystem composed of two microfluidic
channels mimicking the lumen-capillary tissue-tissue interface lined by human small
intestinal villi and inhabited by viable human gut microbes that mimics the
complex three-dimensional microarchitecture and function of living intestine.
The physiological microenvironment of small intestine was recreated by
trickling fluid flow and exerting cyclic mechanical strains that emulate physiological
peristalsis-like motions and flow. We leveraged this humanized Gut-on-a-Chip
microsystem to independently control potential contributors to human intestinal
inflammation and epithelial injury by applying different levels of biological
and physiological complexity. We found that pathological destruction of
intestinal villi resulted when villi are simultaneously challenged to lipopolysaccharide
or non-probiotic bacteria in the lumen and immune cells in the vascular side,
respectively. This complex cross-talk induced the secretion of four
proinflammatory cytokines that were necessary and sufficient to cause gut
injury, which were significantly suppressed by co-administering probiotics or antibiotics.
By ceasing peristalsis-like motions while maintaining luminal flow, lack of
epithelial distortion was shown to trigger bacterial overgrowth, similar to
that observed in patients with ileus and inflammatory bowel disease. Hence, our
results can provide new insights into molecular and cellular mechanisms of
intestinal inflammatory disease and lead to the development of a humanized <em>in vitro</em> disease model that faithfully
mimics human intestinal pathophysiology and determines the efficacy and
toxicity of new drugs. </p><p><img src="/uploads/552daf4a0cd1a.PNG" unselectable="on"></p><p><img src="/uploads/552daf7bda62d.PNG" unselectable="on"></p>
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