Background: Bacteria such as Staphylococcus aureus induce myocardial dysfunction in vivo. To rectify conflicting
evidence about the role of TLR2 signaling and cardiac dysfunction, we hypothesized that the specific TLR2 agonist
purified lipoteichoic acid (LTA) from S. aureus contributes to cardiac dysfunction in vitro and in vivo.
Methods: Wildtype (WT-) and TLR2-deficient (TLR2-D) mice were challenged with LTA and in comparison with
equivalent doses of lipopolysaccharide (LPS) and CpG-oligodeoxynucleotide (CpG-ODN). TLR2-expression, NFκB as
well as cytokine response were determined. Sarcomere shortening of isolated cardiomyocytes was analyzed in vitro
and cardiac function in vivo after stimulation with LTA.
Results: LTA induced up-regulation of TLR2 mRNA, activation of NFκB and cytokine expression within 2–6 h in WT-,
but not in TLR2-D hearts. Cytokines were also elevated in the serum. LPS and CpG-ODN induced a more severe
cardiac inflammation. In vitro incubation of cardiomyocytes with LTA reduced sarcomere shortening via NO at
stimulation frequencies ≤ 8 Hz only in WT cells. However, hemodynamic parameters in vivo were not affected by
Conclusions: LTA induced cardiac inflammation was relatively weak and sarcomere shortening was reduced only
below physiological heart rates. This may explain the apparent contradiction between the in vivo and in vitro LTA
Keywords: LTA, TLR2, Sepsis, Cardiac dysfunction, Cardiac contractility