Exposure to second-hand tobacco smoke has been linked to numerous health problems, including poor wound healing, but the underlying molecular mechanisms have remained unclear. Research in the April 5
“This has the possibility of being a quite important paper,” said Richard Robbins, from the Carl T. Hayden VA Medical Center in Phoenix. “The concept that smoke increases fibroblast survival is very appealing, since smoke-induced lung injury is a mixture of both injury and repair [fibrosis],” said Robbins, who was not involved in the study.
“It is known that people exposed to cigarette smoke suffer from impaired healing,” said Manuela Martins-Green, from the University of California, Riverside, and senior author of the study. “We were interested in determining the effects of levels of smoke that are found in tissues of people exposed to second-hand smoke on fibroblasts because these cells are the 'work horses' of the healing process,” she told
Martins-Green and colleagues used a mixture of components found in second-hand smoke, also termed side-stream whole (SSW) smoke. The addition of this solution to cultures of chicken embryonic fibroblasts at high concentrations caused the cells to die. At lower concentrations, it did not kill the cells, but instead activated a selection of stress response proteins (e.g., PKB/Akt, grp78, p53), suggesting that lower levels of SSW smoke caused increased cell survival.
“That higher concentrations killed the cells did not surprise us, but that lower levels increased survival did catch us by surprise,” said Martins-Green. “We expected that the cells exposed to lower levels would be sick and recover with difficulty when the smoke was removed. What we found was that they recovered extremely well.”
SSW smoke exposure also changed fibroblast morphology, suggesting it could also have an affect on cell motility mechanisms. Using a ring migration assay, the authors discovered that SSW-treated cells migrate poorly, a finding that correlated with increased stress fiber formation and focal adhesion plaque formation.
“Second-hand smoke may delay wound repair because of the inability of the fibroblasts to migrate into the wounded area, leading to an accumulation of these cells at the edge of the wound,” Martins-Green said. “Furthermore, the increase in cell survival coupled to the decrease in cell migration can lead to a build-up of tissue, thereby causing fibrosis and excess scarring.”
“The premise is interesting,” said Carol Basbaum, professor at the University of California, San Francisco, who was not involved in the study. She suggested that the effect second-hand smoke has on fibroblast motility “could be responsible for impaired wound healing in people exposed to second-hand smoke.” However, she cautioned that the work is preliminary and still in need of more rigorous testing.
What impact will the research have on our understanding of the effects of second-hand smoke? Martins-Green said she hopes that it will not only help to better understand how smoke effects wound healing, but also further the social implications of smoking.
“We would [hope] that people of older age are respectful of others who do not smoke, since second-hand smoke may have great impact on health and in the ability to heal,” she said.