Why passive smoking hinders healing

Being exposed to high levels of 'second-hand' smoke can reduce the speed at which wounds heal, leading to a lack of healing or greater levels of scarring. A study published in the journal BMC Cell Biology this week may begin to explain why: when cells are exposed to smoke, their ability to migrate towards the site of damage is compromised.

The study, carried out by researchers from University of California, Riverside, examined the effects of 'second-hand' smoke on fibroblasts, cells that play a major role in wound healing. They found that, among other things, exposure to smoke altered the arrangement of the cells' cytoskeleton increasing the cells' adhesive properties and thus reducing their motility.

The researchers write: "These effects can contribute to abnormal healing and may explain why people who are consistently exposed to 'second-hand' smoke suffer from slow healing and excessive scarring of wounds, much like smokers themselves."

The research team, led by Professor Manuela Martins-Green, bubbled smoke from the lit end of cigarettes through cell culture media to form a solution containing the major components of 'second-hand' smoke. They then diluted the 'smoky media' until the smoke components reached the levels found in the tissues of passive smokers.

When they added this media to fibroblast cells cultured in vitro, the researchers saw that the cells became more elongated and that they separated from one another. By studying components of the cytoskeleton in more detail the researchers saw that exposure to smoke increased the level of one particular cytoskeletal component, actin, inside the cell. It also increased the number of points at which the cell stuck to the Petri dish, sites that could be identified by the presence of 'focal adhesion plaques'.

In a separate experiment, the researchers showed that fibroblasts that had been cultured in the 'smoky medium' were less mobile than control cells.

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Contact: Gemma Bradley
BioMed Central

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