Second-hand smoke ‘triggers inflammatory response in lungs’

WASHINGTON - Researchers at the University of Colorado-Denver have found that second-hand smoke triggers a complex inflammatory response in rat lungs.

The team found that two months of exposure to second-hand smoke were enough to cause significant changes in the rats’ lung tissue, and the results were even more profound in rats exposed for four months.

The researchers observed enlargement in the tiny sacs where oxygen-carbon dioxide exchange takes place during respiration. This suggests that the alveolar structure had begun to break down, much as it does in early emphysema.

They also noted increased numbers of white blood cells called macrophages in the alveolar space of the rats exposed to second-hand smoke, indicating that the rats’ bodies had mounted an immune response.

Adelheid Kratzer also noted that the macrophages “had an odd shape, as if they had engulfed particles, which might impair their function.”

There were also increased levels of interleukin-18, a cytokine produced by macrophages and associated with strong inflammatory reactions and tissue destruction.

Endothelial cells, which serve as a barrier between the inner space of the blood vessel and surrounding tissue and control the transit of white blood cells into and out of the bloodstream, appeared to have decreased in growth due to the smoke.

The team noted that treatment with alpha-1-antitrypsin, a protein made in the liver that is normally present in the blood and protects the lungs and other tissue from the damaging effects of tissue-degrading enzymes produced by inflammatory cells. In humans, a deficiency of this protein causes lung disease. (ANI)