Effects of Cigarette Smoke in Mice Wound Healing is Strain Dependent

Histology and Embryology Department, State University of Rio de Janeiro, Rio de Janeiro, Brazil.
Toxicologic Pathology (Impact Factor: 2.14). 02/2007; 35(7):890-6. DOI: 10.1080/01926230701459986
Source: PubMed


It has been clinically and experimentally shown that cigarette smokers suffer from impaired wound healing, but the mechanisms that lead to the alterations are not well understood. The aim of this study was to investigate if the effects of cigarette smoke exposure on excisional cutaneous wound healing are different depending on the strain (Swiss, BALB/c and C57BL/6 mice) studied. Male mice were exposed to smoke of nine whole cigarettes per day, 3 times/day, daily, for 10 days. In the 11th day a full-thickness excisional wound was performed. Control group was sham-exposed and also had a full-thickness excisional wound. The cigarette smoke exposure protocol was performed until euthanasia. Animals were euthanatized 14 days after wounding. Wound contraction was evaluated 7 and 14 days after lesion. Sections were stained with hematoxylin-eosin, Sirius red or toluidine blue and immunostained for alpha-smooth muscle actin. Smoke exposed animals presented delay in wound contraction, in fibroblastic and inflammatory cells recruitment and in myofibroblastic differentiation; those alterations were strain dependent. Cigarette smoke exposure also affected mast cells recruitment and neoepidermis thickness. In conclusion, the present study demonstrated that the effects of cigarette smoke in mice cutaneous wound healing are related to mice strain studied.

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Available from: Luís Cristóvão Porto
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    • "It is known that mast cells, which are found in conjunctive tissue, are mobilized during wound healing and participate in all phases of the process [23], especially in the inflammatory phase, because these cells are the first to release inflammatory mediators involved in vasodilatation [1, 23] and the recruitment and increased survival of leukocytes [23]. However, it has been shown that prolonged mobilization of mast cells until 21 days after wound formation can damage the formation of granulation tissue [24] and that an excess of mast cell mediators (such as kinases) may delay the migration of epithelial cells [25, 26]. According to Barroso et al. [23], propolis has potential anti-inflammatory effects in acute inflammation and reduces the number of mast cells, but it does not have the same effect in the later stages of repair. "
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    • "In each strain, animals were separated in control (n ¼ 10) and smoke-exposed (n ¼ 14) groups. Smoke-exposed groups had the whole body exposed, in an inhalation chamber, to a smoke–air mixture of commercial filtered Virginia cigarettes, three times per day, seven days per week, during the entire experiment, as previously described (Cardoso et al. 2007; Valenca et al. 2004). The cigarette smoke exposure protocol started ten days before the excisional wound and continued until the end of the experiment. "
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    • "Mouse strain variations in inflammation and wound healing have also been reported. The affect of cigarette smoke on the healing of skin wounds was tested in BALB/c, C56BL6, and Swiss mice (Cardoso, et al., 2007). Contraction of skin wounds in BALB/c and C57BL6 was inhibited compared to Swiss mice and each strain had is own distinct inflammatory response to injury and to cigarette smoke. "
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