Protein Mediates Damage from Tobacco Pollutants
Compounds lead to inflammation and respiratory hypersensitivity
MONDAY, June 23 (HealthDay News) -- Compounds present in cigarette smoke responsible for inflammation of lung nerve endings and respiratory hypersensitivity mediate their effects via an excitatory ion channel, according to a report published online June 20 in the Journal of Clinical Investigation.
Eunice Andre, from the University of Ferrara in Italy, and colleagues investigated whether two compounds present in cigarette smoke -- crotonaldehyde and acrolein -- had a role in stimulating the neurogenic inflammatory response observed in rodent airways after exposure to cigarette smoke.
The researchers found that cigarette smoke, or the compounds, activated signaling pathways in guinea pig jugular ganglia neurons and promoted contraction of guinea pig bronchi, which could be blocked by inhibiting TRPA1, an excitatory ion channel. Treatment also promoted neuropeptide release from guinea pig airway tissue. Treatment with cigarette smoke or the compounds had no effect on signaling in neurons from mice lacking TRPA1.
The study "point[s] to a role for TRPA1 channels in response to pollutants, whether they originate from cigarette smoke, oxidizing agents, or from other irritants in the air," Sidney A. Simon, Ph.D., and Wolfgang Liedtke, M.D. Ph.D., from Duke University Medical Center in Durham, N.C., write in an accompanying editorial.
The authors of the editorial have received financial support from Philip Morris USA and Philip Morris International.