Thymosin β4 protects C57BL/6 mice from bleomycin‐induced damage in the lung

Abstract

This is the first report that shows a Tβ4 protective role in lung toxicity associated with BLEO in a mouse model. Future studies are needed to assess its putative antifibrotic properties.

Effects of thymosin β4 and its N-terminal fragment Ac-SDKP on TGF-β-treated human lung fibroblasts and in the mouse model of bleomycin-induced lung fibrosis

“…In contrast to the protective result of Tb4 on the early fibrosis at 7 days after bleomycin instillation as previously described [4,5], treatment with Tb4 failed to protect bleomycin-treated mice from lung fibrosis observed at 14 and 21 days. As shown in Figure 1, the histological features of the Sham and Sham + Tb4 mice lungs are identical.…”

“…Accordingly, our recent in vivo studies demonstrated wide protective effects of Tb4 in mice treated with bleomycin, and in particular significant inhibitory results on bleomycin-induced inflammation and on early fibrosis at 7 days [4,5]. By using the same dose, route and scheduling of previous researches, in this current study we addressed the potential role of Tb4 in halting progression of fibrosis.…”

“…In recent papers, we demonstrated that Tb4 exerts a broad protective role in mice treated with bleomycin, with specific inhibitory effects on both inflammation and initial fibrosis [3][4][5]. Pulmonary fibrosis occurs in a variety of clinical settings as heterogeneous disease sometimes taking place in the context of connective tissue diseases that may be helped by immunosuppressive therapies and in some cases reversible [6].…”

The role of thymosin-β4 in kidney disease

“…Thymosinb4 can also bind to stabilin-2, a membrane receptor involved in the engulfment of apoptotic cells [4]. The ability of thymosin-b4 to regulate cell movement and turnover has led to studies showing that it can stimulate coronary vasculogenesis and angiogenesis [5] and regulate inflammation and fibrosis in mouse models of lung, heart and cornea injury [6][7][8]. Thymosin-b4 derivatives have similar properties.…”

Update on scleroderma-associated interstitial lung disease

“…A peptide derived from its aminoterminal end, Ac-sdkp, is responsible for the antifibrotic effects of angiotensin converting enzyme inhibitors(42). Conte et al (43) found that exogenous Tβ4 is protective in mice receiving intratracheal bleomycin. In a subsequent paper, they attribute these findings to Tβ4-mediated reduction in the numbers of IL-17 producing cells in circulation as well as decreased IL-17 levels in the lung tissue(44).…”