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Translocates into the Myocardium and Forms Unique Microlesions That Disrupt Cardiac Function
Hospitalization for community-acquired pneumonia carries a documented risk for adverse cardiac events. These occur during infection and contribute to elevated mortality rates in convalescent individuals up to 1 year thereafter. We describe a previously unrecognized pathogenic mechanism by which Streptococcus pneumoniae, the leading cause of community-acquired pneumonia, causes direct cardiotoxicity and forms microscopic bacteria-filled lesions within the heart. Microlesions were detected in experimentally infected mice and rhesus macaques, as well as in heart sections from humans who succumbed to invasive pneumococcal disease (IPD). Cardiac microlesion formation required interaction of the bacterial adhesin CbpA with host Laminin receptor and bacterial cell wall with Platelet-activating factor receptor. Microlesion formation also required the pore-forming toxin pneumolysin. When infected mice were rescued with antibiotics, we observed robust signs of collagen deposition at former lesion sites. Thus, microlesions and the scarring that occurs thereafter may explain why adverse cardiac events occur during and following IPD.
Vyšlo v časopise: Translocates into the Myocardium and Forms Unique Microlesions That Disrupt Cardiac Function. PLoS Pathog 10(9): e32767. doi:10.1371/journal.ppat.1004383
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004383Souhrn
Hospitalization for community-acquired pneumonia carries a documented risk for adverse cardiac events. These occur during infection and contribute to elevated mortality rates in convalescent individuals up to 1 year thereafter. We describe a previously unrecognized pathogenic mechanism by which Streptococcus pneumoniae, the leading cause of community-acquired pneumonia, causes direct cardiotoxicity and forms microscopic bacteria-filled lesions within the heart. Microlesions were detected in experimentally infected mice and rhesus macaques, as well as in heart sections from humans who succumbed to invasive pneumococcal disease (IPD). Cardiac microlesion formation required interaction of the bacterial adhesin CbpA with host Laminin receptor and bacterial cell wall with Platelet-activating factor receptor. Microlesion formation also required the pore-forming toxin pneumolysin. When infected mice were rescued with antibiotics, we observed robust signs of collagen deposition at former lesion sites. Thus, microlesions and the scarring that occurs thereafter may explain why adverse cardiac events occur during and following IPD.
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