A macrolide antibiotic, roxithromycin, inhibits the growth of nasal polyp fibroblasts

Recently, the efficacy of macrolide antibiotics in cystic fibrosis and bleo mycin-induced lung injury was reported Nasal polyposis is a chronic inflamm atory disease of the upper airway characterized by structural abnormalities including stromal fibrosis, Fibroblasts ave resident cells thought to play an important role in the development of fibrosis. Although the effect of R oxithromycin (RXM) on inflammatory cells is well known, there is no evidenc e on the effect of RXM on fibroblasts. The purpose of the present study was two-fold: to examine the effect of RXM on the growth of fibroblasts in vit ro and to examine the effect of RXM on the proliferation of fibroblasts in vivo. Nasal polyp fibroblast lines were generated from untreated patients, and those who were treated with RXM (300 mg/day) for one month before biops y. Nasal polyp fibroblast lines from untreated patients were cultured for 7 2 hours with or without RXM, and the direct effect of RXM on fibroblast gro wth in vitro was examined by cell counting and H-3 thymidine uptake. Next, we examined the in vivo effect of RXM on nasal polyp fibroblasts (NPFs) by comparing the growth characteristics of NPF lines from RXM treated and untr eated patients. Finally, we examined the proliferating rate of NPF lines fr om the same patient before and after treatment with RXM. NPF lines that wer e treated with RXM exhibited a lower proliferating rate in vitro as compare d to those that were not treated with RXM. Treatment of NPF lines with RXM suppressed the proliferation of fibroblasts in a dose-dependent manner. In addition, NPF lines from patients treated with RXM exhibited a lower prolif erating rate in vitro as compared to NPF lines from the same patient taken before RXM treatment. We demonstrated that RXM directly suppressed nasal po lyp fibroblast proliferation, and that this effect of RXM on fibroblast gro wth was persistent, indicating that RXM may prevent the progression of nasa l polyposis by inhibiting the development of fibrosis.