Mitochondrial DNA and Streptococcus pneumoniae Infection – Induction of Immuno-inflammatory Response

Streptococcus pneumoniae, or pneumococcus, is one of the leading causes of morbidity and mortality associated with lower respiratory infections. Usually, it colonizes asymptomatically the human upper respiratory tract, but it can eventually migrate to other body sites to cause invasive and non-invasive diseases. The polysaccharide capsule (CPS) is the main pneumococcal virulence factor and it is used in the currently available vaccines against this pathogen. However, novel therapeutic and prevention approaches are urgently needed to target emergent non-vaccine serotypes, especially those associated with antimicrobial resistance. Besides CPS, pneumococcus has several other virulence factors that contribute to its pathogenesis, including surface proteins (e.g., CbpA), the pore-forming toxin pneumolysin (PLY), as well as enzymes that produce hydrogen peroxide (H2O2). Here, we describe the pathogenesis of pneumococcal infections as well as host cell molecular signaling, focusing on major molecules responsible for host cell invasion and translocation, and disturbance of mitochondrial function, resulting in mitochondrial DNA (mtDNA) leakage, inflammation and tissue damage. Understanding molecular and immunoinflammatory mechanisms underlying pathogenesis and pathogen-host cell interactions is crucial to developing novel approaches to prevent and treat pneumococcal diseases. 

Keywords: Mitochondrial DNA, Pneumococcus, Streptococcus pneumoniae.