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Deadly disease mimicked in organ-on-a-chip

09 Nov 2012

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Researchers at Harvard University's Wyss Institute for Biologically Inspired Engineering have found a way to mimic a lung disease called pulmonary oedema by lining a microchip with living human cells. They used this device to try experimental therapies and to study drug toxicity in relation to the deadly disease. The breakthrough "organ-on-a-chip" could pave the way towards the replacement of expensive, traditional approaches to drugs testing.

"Major pharmaceutical companies spend a lot of time and a huge amount of money on cell cultures and animal testing to develop new drugs," says Donald Ingber, M.D., Ph.D., founding director of the Wyss Institute and senior author of the study, "but these methods often fail to predict the effects of these agents when they reach humans."

The lung-on-a-chip device is a crystal clear, flexible polymer about the size of a memory stick that contains hollow channels fabricated using computer microchip manufacturing techniques. Two of the channels are separated by a thin, flexible, porous membrane that on one side is lined with human lung cells from the air sac and exposed to air. Human capillary blood cells are placed on the other side with medium flowing over their surface. A vacuum applied to side channels deforms this tissue-tissue interface to re-create the way human lung tissues physically expand and retract when breathing.


lung-on-a-chip

This "lung-on-a-chip" mimics the complicated mechanical and biochemical behaviours of a human lung.


Surprise results
Wyss Technology Development Fellow Dongeun Huh, Ph.D., who also holds appointments at Boston Children's Hospital and Harvard Medical School, studied a cancer chemotherapy drug called interleukin-2—or IL-2 for short—in the lung-on-a-chip. A major toxic side effect of IL-2 is pulmonary oedema, which is a life-threatening condition in which the lungs fill with fluid and blood clots.

When IL-2 was injected into the blood channel of the lung-on-a-chip, fluid leaked across the membrane and two tissue layers, reducing the volume of air in the other channel and compromising oxygen transport—just as it does in lungs of human patients when it is administered at the equivalent doses and over the same time course. Blood plasma proteins also crossed into the air channel, leading to the formation of blood clots in the air space, as they do in humans treated with IL-2.

But one result came as a surprise.

It turns out the physical act of breathing greatly enhances the effects of IL-2 in pulmonary oedema—"something that clinicians and scientists never suspected before," Ingber says. When the team turned on the vacuum attached to the chip to simulate breathing, it increased fluid leakage more than three-fold when treated with the clinically relevant IL-2 dose, and the Wyss team confirmed that the same response occurs in an animal model of pulmonary oedema. This result could suggest that doctors treating patients on a respirator with IL-2 should reduce the tidal volume of air being pushed into the lungs, for example, in order to minimise the negative side effects of this drug.

"In just a little more than two years, we've gone from unveiling the initial design of the lung-on-a-chip to demonstrating its potential to model a complex human disease, which we believe provides a glimpse of what drug discovery and development might look like in the future," Ingber says.




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