Table 2.

Summary of pneumolysin-mediated mechanisms of immunosuppression and cardiotoxicity in the pathogenesis of severe myocardial dysfunction.

Mechanism	References
Ply-mediated suppression of the protective activities of infiltrating and resident sentinel cardiac macrophages via induction of necroptosis following adherence of the pathogen to the vascular endothelium of myocardial capillaries	[68,69,70]
Following invasion of the myocardium the pneumococcus becomes established in intra-cardiac microlesions in which it transitions to a biofilm-forming, high Ply-producing phenotype	[71,73,74]
Cardiotoxicity results from interaction of the pneumococcal adhesins PspA, CbpA, and Psrp with cardiomyocytes, resulting in exposure of these cells to Ply, leading to cell death and myocardial dysfunction	[75,76]

Abbreviations: Ply (pneumolysin); PspA (pneumococcal surface protein A); CbpA (choline-binding protein A); Psrp (pneumococcal serine-rich repeat protein).