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Over the past decades there has been an ongoing debate whether preventing lower respiratory tract infections through pneumococcal (polysaccharide) vaccination (PPV) could decrease the risk of venous and arterial thrombosis. This hypothesis is mainly based on findings from animal experiments indicating that systemic inflammation and infections accelerate atherosclerosis.1 Recent circumstantial evidence from an observational study in patients with persistent immune activation (eg, due to HIV infection) suggests that systemic inflammation may also accelerate atherosclerosis in humans.2 In support of this, multiple studies have shown that circulating markers of inflammation, such as C reactive protein, interleukin 6 and D-dimer predict the risk of arterial thromboembolic events in humans.3 Clearly, systemic inflammation is not a constant but varies in response to proinflammatory stimuli. Intermittent changes caused by acute infections have been linked to short-term increases in the risk of vascular events in large observational studies.4 Although the pathogenesis may differ, the same associations have also been made between venous thromboembolic events, and systemic inflammation and infections.4 ,5 Interestingly, in addition to preventing lower respiratory tract infections, PPV-induced antibodies have been proposed to possess other potentially beneficial effects. In vitro studies have suggested molecular mimicry between the immunodominant phosphorylcholine epitopes of oxidised phospholipids of oxidised low-density lipoprotein and the phosphorylcholine moiety of Streptococcus pneumoniae …
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