Lung-on-a-chip technology could lead to improved treatments for chronic obstructive pulmonary disease (COPD), a smoking related condition that’s thought to be the third leading cause of death worldwide.
Developed by a team from Harvard University’s Wyss Institute for Biologically Inspired Engineering, the technology consists of a lab-on-a-chip device which supports cells from normal or diseased human lungs and an instrument that “breathes” cigarette smoke in and out over these chips.
Using the device, the research team was able to recreate and analyse the effects of smoking at the molecular, cellular, and tissue level to gain a better understanding of the damage caused by COPD and identify potential therapies.
“It’s one of the lung diseases that has very few therapeutics available in the market,” said researcher Kambez H. Benam. “Most of the drugs given are to control the symptoms; there is no cure to reverse or prevent disease progression.”
To understand how smoking affects the small airways damaged in COPD, the researchers first built a lung airway-on-a-chip. These devices are made of a clear flexible rubber the size of a computer memory stick lined with living human cells.
A smoking machine, which mimics the action of a human smoker, connects to the airway-on-a-chip and a microrespirator, which acts as a diaphragm pulling air and smoke across the chip and pushing it out. Software determines, among other variables, how many puffs the smoking machine takes per cigarette and how many breaths between puffs.
The researchers showed that when exposed to smoke, the airway-on-a-chip experienced changes in oxidation-reduction pathways and gene expression profiles that matched those found in human smokers.
Using automated image processing, they also showed that on chips exposed to smoke, cilia – the wafting hairs that line that respiratory system – in some areas beat normally but in other areas beat at much reduced rates, providing insights into what happens in smokers’ lungs.
The team also tested the effects of e-cigarettes and found less evidence of changes in oxidation-reduction pathways but similar changes in cilia beat patterns.