Elevated local TGF-β1 level predisposes a closed bone fracture to tuberculosis infection

Abstract

Tuberculosis (TB) occurring after a closed bone fracture in the patient with no history of TB and no evidence of TB infection at the time of initial fracture is a rare entity. Transforming growth factor-beta 1 (TGF-β1) is a ubiquitous growth factor that is implicated in the regulation of the proliferation, differentiation, migration, and survival of many different cell types. Recent studies have demonstrated that the local level of TGF-β1 in bone is significantly elevated during fracture healing and TGF-β1 plays an important role in TB progression. Given the above background, we hypothesize that elevated local TGF-β1 level predisposes a closed bone fracture to TB infection. This was supported by conclusions drawn from literature reviews: (1) the local level of TGF-β1 in bone is significantly elevated during fracture healing; (2) TGF-β1 inhibits T lymphocyte activation; (3) TGF-β1 is a potent macrophage-deactivating molecule; (4) TGF-β1 suppresses the production and activity of some proinflammatory cytokines.