Collagen-targeted PET/CT imaging of tuberculosis patients

<title>Extract</title> In addition to being the leading cause of death from a single infectious disease, tuberculosis (TB) causes chronic respiratory sequelae, including impaired lung function, in over 50% of TB survivors [1, 2]. Pulmonary TB results in fibrosis and cavitation in up to 84% and 70% of patients after treatment completion, respectively [3]. TB-associated lung damage involves extra-cellular matrix breakdown by host matrix metalloproteinases (MMPs) that degrade lung collagen [4, 5]. Despite its relevance to disease pathogenesis and patient outcomes, limited data on matrix remodeling during active TB are available in humans. Higher levels of airway MMP-1 and MMP-2 correlate with pulmonary cavitation [6], and a small randomized trial found that using the MMP inhibitor doxycycline during TB treatment was associated with decreased cavity volume [7]. Therefore, host-directed therapies (HDTs) modifying matrix remodeling and aberrant fibrosis could improve post-TB outcomes. However, such interventions would likely be most successful in patients presenting with greater profibrotic activity and collagen deposition.