Further evidence for the role of fibrosis in the pathobiology of rhinophyma.

Abstract

Recent evidence suggests that fibrosis may play an important role in the pathobiology of rhinophyma. The fibrogenic cytokine transforming growth factor (TGF)-beta2 has been reported to be up-regulated in rhinophyma tissue. Of the three common isoforms of TGF-beta, TGF-beta1 and TGF-beta2 are considered fibrogenic, whereas TGF-beta3 has antiscarring properties. To provide further evidence for the role of fibrosis in the pathobiology of rhinophyma, specimens from 8 patients with rhinophyma were compared with nine specimens of normal nasal skin. Immunohistochemistry was used to compare intensity levels of TGFbeta1 and TGFbeta3 proteins, and quantitative reverse transcription-polymerase chain reaction was used to determine messenger ribonucleic acid (mRNA) expression levels of TGFbeta1 and TGFbeta3. TGF-beta1 was elevated significantly in rhinophyma tissue (p < 0.001), whereas TGF-beta3 was no different in the rhinophyma specimens compared with normal nasal skin (p = 0.06). TGFbeta1 mRNA expression was five-fold higher in rhinophyma tissue compared with normal skin (p < 0.001). The mRNA expression of TGF-beta3 was the same for both pathological and normal tissue (p < 0.09). These data, together with previously published observations, present further evidence that fibrosis mediated by the fibrogenic cytokines TGFbeta1 and TGFbeta2 play a role in the pathobiology of rhinophyma and suggest a means of treatment by neutralizing or down-regulating these cytokines.