Are TNF-α and IL-1β the cause of post-burn hypertrophic scar tissue one year later?

Introduction. Post-burn hypertrophic scar tissue (H) is characterized by increased collagen synthesis, cellular growth and cell turnover. Its clinical characteristics exhibit aspects of chronic local inflammation, but the mechanism of its pathogenesis has not been clearly elucidated. In chronic skin inflammation, proinflammatory and profibrogenic cytokines play an important role in producing skin dysfunction. In this study, we examined changes in tumor necrosis factor (TNF)-α and interleukin (IL)-1β mRNA expression and its presence in post-burn hypertrophic scars. Results obtained in normotrophic scar tissue (N) were compared to results obtained in normal skin (NS). Materials and Methods. Skin biopsies were obtained from 15 patients with (H) who presented burns on over 10% of their skin surface, more than a year post-injury. N were obtained from 17 patients who experienced scarring in optimal conditions. NS were obtained from 11 patients who underwent cosmetic or reconstructive surgery. We performed histopathologic analysis with routine processing. TNF-α and IL-1β mRNA expression levels on all three types of biopsy were obtained by RT-PCR and in situ hybridization. Results. TNF-α and IL-1β mRNA expression was highly coordinated and was very similar in all the tissues processed and our histopathologic analysis yielded relatively low inflammatory infiltrate cell. But according to a semiquantitative analysis RT-PCR, TNF-α and IL-1β mRNA expression was significantly decreased in hypertrophic scars when they were compared to NS and N. Conclusions. These results suggest, that there not a differential expression TNF-α and IL-1β mRNA in hypertrophic scars a one year post injury. Interestingly, the keratinocytes showed minus expression of IL-1β mRNA compared to other cell types, which suggests that they may play an important role in post-burn skin repair processes.