The Impact of Aging and Toll-like Receptor 2 Deficiency on the Clinical Outcomes of Staphylococcus aureus Bacteremia

Staphylococcus aureus (S. aureus) causes a broad range of infections. Toll-like receptor (TLR) 2 senses the S. aureus lipoproteins in S. aureus infections. Aging raises the risk of infection. Our aim was to understand how aging and TLR2 affect the clinical outcomes of S. aureus bacteremia. Four groups of mice (wild type/young, wild type/old, TLR2(-/-)/young, and TLR2(-/-)/old) were intravenously infected with S. aureus, and the infection course was followed. Both TLR2 deficiency and aging enhanced the susceptibility to disease. Increased age was the main contributing factor for increased mortality rates and changes in spleen weight, whereas other clinical parameters, such as weight loss and kidney abscess formation, were more TLR2 dependent. Importantly, aging increased mortality rates without relying on TLR2. In vitro, both aging and TLR2 deficiency down-regulated cytokine/chemokine production of immune cells with distinct patterns. In summary, we demonstrate that aging and TLR2 deficiency impair the immune response to S. aureus bacteremia in distinct ways. In Staphylococus aureus bacteremia mouse model, aging and TLR2 deficiency impair the immune responses in distinct patterns. Mortality was more controlled by aging, whereas weight loss and kidney abscess were more TLR2 dependent. Aging increased mortality independent of TLR2 expression.

Automated summary

In this study using a mouse model of Staphylococcus aureus bacteremia, aging and TLR2 deficiency were found to impair immune responses in distinct patterns. Mortality was mainly controlled by aging, while weight loss and kidney abscess formation were more TLR2 dependent. Aging increased mortality independent of TLR2 expression.