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.

During normal wound healing, fibroblasts migrate into the area of damaged tissue and secrete growth factors, cytokines and extra-cellular matrix components. If the cells are unable to migrate, they will remain concentrated at the edge of the wound, preventing the wound from closing properly. If, in addition, the fibroblasts deposit excess extra-cellular matrix components at the edge of the wound, abnormal scars are likely to form.

"These findings have led us to further our studies in a system that more closely mimics the in vivo environment. We are currently using a mouse model system and special chambers, where the mice smoke, to attempt to correlate our in vitro findings with in vivo results," write the researchers.

Preliminary results suggest that mice that have been exposed to smoke for 6 months are indeed slower at healing wounds. Seven days after mice were wounded using a 5mm diameter hole-punch, wounds of 'non-smoking' mice were 95% closed, whereas wounds of 'smokers' were only 85% closed.

In 'second-hand' smoke, many components are more concentrated than in first-hand smoke. For example, the concentrations of nicotine, tar, nitric oxide and carbon monoxide levels are at least twice as high. The researchers hope that their work will: "lead eventually to the realization that 'second-hand' smoke exposure can be very damaging."


This press release is based on the following article:
Effects of 'second-hand' smoke on structure and function of fibroblasts cells that are critical for tissue repair and remodelling
Lina Wong, Harry Miguel Green, Jo Ellen Feugate, Madhav Yadav, Eugene A Nothnagel and Manuela Martins-Green
BMC Cell Biology 2004, 5:12
To be published 5 April 2004

Upon publication this article will be available free of charge according to BMC Cell Biology's Open Access policy at http://www.biomedcentral.com/1471-2121/5/12/

Please mention the journal in any story you write, and link to the article if you are writing for the web.


For further information about this research contact Professor Manuela Martins-Green by email at [email protected] by phone on 909-787-2585.

Alternatively, or for further information about BMC Cell Biology or Open Access publishing, contact Gemma Bradley, by phone on 44-207-323-0323 or email at [email protected].

Source: Eurekalert & others

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