• Corpus ID: 18371886

Dongeun Huh Lung-ona-Chip Microdevice Induced Pulmonary Edema in a − A Human Disease Model of Drug Toxicity

@inproceedings{Huh2012DongeunHL,
  title={Dongeun Huh Lung-ona-Chip Microdevice Induced Pulmonary Edema in a − A Human Disease Model of Drug Toxicity},
  author={Dongeun Huh and Daniel C Leslie and Benjamin D. Matthews and Jacob P. Fraser and Samuel Jurek and Geraldine A. Hamilton and K S Thorneloe and Michael Allen McAlexander and Donald E. Ingber},
  year={2012}
}

• D. Huh, Daniel C Leslie, +6 authors D. Ingber
• Published 2012
• Medicine, Biology

could affect patient health. with the goal of one day being able to rapidly screen many drugs and conditions that −− heart, liver, pancreas, etc. −− (this issue). The next step is to hook this lung up to other chip-based organs et al. animals in a study by Thorneloe edema. The beneficial effects of GSK2193874 still need to be confirmed in humans, but were preliminary validated in in response to IL-2 and mechanical strain but also successfully predicts the activity of a new drug for pulmonary have recreated the human lung on a microfluidic chip and shown that it not only mimics lung function et al. Huh patients with pulmonary edema who are being mechanically ventilated. activated by mechanical strain. This drug inhibited leakage, suggesting that it would be a viable treatment option for pulmonary disease model against a new pharmacological agent, GSK2193874, which blocks certain ion channels induced vascular leakage. Lastly, the authors tested their − stabilized the endothelial junctions and inhibited IL-2 pulmonary barrier even further and led to a threefold increase in leakage. As expected, the addition of angiopoietin-1 pulmonary leakage, also known as ''edema.'' Cyclic mechanical strain introduced with IL-2 compromised the fluid started to leak into the air compartment. This process reproduces what is seen in the clinic, where IL-2 induces breathing motion of the lung. When Huh and colleagues added interleukin-2 (IL-2) to the microvascular channel, the ''microvascular'' channel was filled with liquid. Vacuum was cyclically applied to the sides of the channels to mimic the membrane. Much like the human lung, the upper ''alveolar'' channel was filled with air, whereas the lower The authors cultured two types of human lung cells in parallel microchannels, which were separated by a thin human lung function in both normal and disease states. effects in humans. Toward a more reliable output, Huh and colleagues developed a ''lung-on-a-chip'' that models Drug testing in animal models is time-consuming, costly, and often does not accurately predict the adverse Pulmonary Edema-on-a-Chip