Airway Damage Caused by Pollutants Airway skade forårsaget af miljøgifte

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. Ny indsigt i, hvordan forurening og cigaretrøg skader luftvejene er stillet til rådighed af Pierangelo Geppetti og kolleger, ved universitetet i Firenze, Italien, der undersøgt virkningerne af disse kemikalier på marsvin luftvejene. Som drøftet, i et ledsagende kommentar ved Sidney Simon og Wolfgang Liedtke på Duke University Medical Center, er det håbet, at disse oplysninger vil hjælpe i udviklingen af terapi til at bekæmpe virkningerne af de forurenende stoffer og måske hjælpe enkeltpersoner med ryge-relaterede sygdomme såsom kronisk obstruktiv lungesygdom og kronisk astma.

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. I undersøgelsen, kemikalier findes i cigaretrøg blev vist sig at aktivere signalering i nerver, der sluttede i luftvejene af marsvin. Disse effekter blev afskaffet ved hjælp af et molekyle, der hæmmede et protein kaldet TRPA1. Overensstemmelse med en central rolle for TRPA1 i sensing kemikalier i cigaretrøg, ingen signalering i nerver, der ender på luftvejene blev observeret hos mus mangler TRPA1 efter eksponering for kemikalier i cigaretrøg. yderligere analyse viste, at alpha, beta-umættede aldehyder var de kemikalier, som aktiveres TRPA1, hvilket tyder på, at de kan bidrage til luftvejs skader, der opstår i ryger-relaterede sygdomme.

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