Most individuals infected with Mycobacterium tuberculosis develop a latent infection, which does not progress to active tuberculosis (TB). This occurs, in part, because infected macrophages recruit immune cells to form a granuloma, isolating the bacteria and preventing its spread. In some individuals, granulomas undergo necrosis and tissue destruction occurs, releasing the bacteria and allowing the development of active disease. In this issue of the JCI, Elkington et al. provide evidence that M. tuberculosis drives the expression of MMP-1, which in turn promotes the collagen breakdown that leads to alveolar destruction in TB. These findings identify putative therapeutic targets for the prevention of TB.
