Fig. 2
From: Acute organ injury and long-term sequelae of severe pneumococcal infections
Cardiac microlesion formation and resolution. Microlesions form in the heart as a result of an individual pneumococcus adhering to the vasculature in the bloodstream and invading the myocardium by crossing vascular endothelial cells. Invaded pneumococci are capable of replicating to form a foci of infection (left panel). Infiltrating macrophages die of H2O2 and pneumolysin-mediated necroptosis preventing further infiltration of immune cells. Additionally, cardiomyocytes undergo necroptotic death leaving “holes” within the heart. The resolution of infection is characterized by the remodeling of cardiac tissue (right panel). This includes the infiltration of fibroblasts that deposit collagen to form long-lasting scar tissue. Microlesion morphology based on high-resolution images of cardiac sections from mice infected with Streptococcus pneumoniae strain TIGR4, shown 30 h post-infection, intraperitoneal challenge