Boston : Harvard scientists have developed a new robotic smoker, an instrument that puffs away cigarettes like a human and is integrated with a lung-on-chip, which may help understand how different people respond to smoke.
While it is well known that cigarette smoking is a major cause of lung disease and a key exacerbating factor for those suffering from chronic obstructive pulmonary disease (COPD), it has not been possible to effectively model its deleterious effects on human lungs under normal breathing conditions.
Researchers at Wyss Institute for Biologically Inspired Engineering at Harvard University in the US developed the instrument that can ‘breathe’ in and out, actively smoke regular and electronic cigarettes much like a human and deliver the smoke to microfluidic organs-on-chips lined by human lung small airway cells isolated from non-smokers or COPD patients.
The integrated smoking system enables a better understanding of smoke-related pathological changes in individual smokers, and could facilitate the discovery of more accurate bio markers and new therapeutic targets.
Classical culture systems with human small airway cells are unable to reproduce the breathing motions of the lung and commonly used laboratory animals cannot reflect human smoking because they breathe through their noses and their inflammatory responses differ from those in humans.
In addition, human clinical studies show great variability in the physiological and biochemical responses between patients, and they usually do not allow direct comparisons of smoke-exposure versus no-exposure in the same individual.
Leveraging the previously developed human lung small airway-on-a-chip model for inflammatory disorders including COPD and asthma, researchers designed a smoking instrument that integrates with the airway chips and recapitulates smoking behaviour with cells derived from healthy people and patients with COPD.
“The device enables us for the first time to compare responses of human small airway tissues, from both normal individuals and COPD patients, before and after they are exposed to cigarette smoke delivered through physiological breathing outside the human body,” said Donald Ingber, professor at Harvard Medical School in the US.
“We can now begin to decipher which cell types, cellular functions and genes contribute to smoke-induced injury in normal lung, as well as during COPD exacerbations in individual patients, and thereby, identify common as well as patient-specific disease factors,” said Ingber.
“We combined the small airway-on-a-chip with a smoking machine that burns cigarettes and a microrespirator that inhales and exhales small volumes of cigarette smoke and fresh air in and out of the epithelium-lined channel in programmable intervals mimicking true smoking behaviour,” said Richard Novak, from the Wyss Institute. MHN MHN
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