同居人の　けむりは傷を　長引かせ

煙害で　傷のなおりが　遅くなる　　　　　　　　　　　　川柳（７）にもどる

受動喫煙は創傷治癒を遅延させる

 Effects of "second-hand" smoke on structure and function of fibroblasts, cells that are critical for tissue repair and remodeling
喫煙者と暮らす子供たちは創傷の治癒に時間がかかる.。
受動喫煙に曝露されると切り傷、やけど、そして感染症の治癒が遅延することがわかった。一般的に細胞は創傷の全面に集まるが、タバコ煙に曝露された子供たちでは細胞は辺縁に集まるので、創傷の治癒が制限される。「何らかの障害がある人間にとって、受動喫煙は直接喫煙と同
様あるいはそれ以上に有害であると言える。
Effects of "second-hand" smoke on structure and function of fibroblasts, cells that are critical for tissue repair and remodeling
Lina S Wong , Harry M Green , Jo Ellen Feugate , Madhav Yadav , Eugene A Nothnagel and Manuela Martins-Green 
BMC Cell Biology 2004, 5:13 

Background

It is known that 'second-hand' cigarette smoke leads to abnormal tissue repair and remodeling but the cellular mechanisms involved in these adverse effects are not well understood. Fibroblasts play a major role in repair and remodeling. They orchestrate these processes by proliferating, migrating, and secreting proteins such as, cytokines, growth factors and extracellular matrix molecules. Therefore, we focus our studies on the effects of 'second-hand' cigarette smoke on the structure and function of these cells. 

Results

We used sidestream whole (SSW) smoke, a major component of "second-hand" smoke, primary embryonic fibroblasts, cells that behave very much like wound fibroblasts, and a variety of cellular and molecular approaches. We show that doses of smoke similar to those found in tissues cause cytoskeletal changes in the fibroblasts that may lead to a decrease in cell migration. In addition, we also show that these levels of cigarette smoke stimulate an increase in cell survival that is reflected in an increase and/or activation of stress/survival proteins such as cIL-8, grp78, PKB/Akt, p53, and p21. We further show that SSW affects the endomembrane system and that this effect is also accomplished by nicotine alone. 

Conclusions

Taken together, our results suggest that: (i) SSW 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, thus preventing the formation of the healing tissue; (ii) the increase in cell survival coupled to the decrease in cell migration can lead to a build-up of connective tissue, thereby causing fibrosis and excess scarring.