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ShareJune 24, 2008 — A new study of the effects of chemicals found in pollution and cigarette smoke on guinea pig airways has provided insight into how these chemicals are likely to damage airways in individuals with in smoke-related diseases such as chronic obstructive pulmonary disease and chronic asthma.
It is hoped that this information will help in the development of therapeutics to combat the effects of pollutants and perhaps help individuals with smoke-related diseases.
New insight into how pollution and cigarette smoke damage airways has been provided by Pierangelo Geppetti and colleagues, at the University of Florence, Italy, who studied the effects of such chemicals on guinea pig airways.
As discussed, in an accompanying commentary, by Sidney Simon and Wolfgang Liedtke, at Duke University Medical Center, it is hoped that this information will help in the development of therapeutics to combat the effects of pollutants and perhaps help individuals with smoke-related diseases such as chronic obstructive pulmonary disease and chronic asthma.
In the study, chemicals found in cigarette smoke were shown to activate signaling in nerves that ended in the airways of guinea pigs. These effects were abolished using a molecule that inhibited a protein known as TRPA1.
Consistent with a central role for TRPA1 in sensing chemicals in cigarette smoke, no signaling in nerves that end in the airways was observed in mice lacking TRPA1 after exposure to the chemicals in cigarette smoke.
Further analysis showed that alpha,beta-unsaturated aldehydes were the chemicals that activated TRPA1, suggesting that they might contribute to the airway damage that occurs in smoke-related diseases.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Pierangelo Geppetti et al. Cigarette smoke--induced neurogenic inflammation is mediated by alpha,beta-unsaturated aldehydes and the TRPA1 receptor in rodents. Journal of Clinical Investigation, June 20, 2008
Note: If no author is given, the source is cited instead.
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