Toll-like receptor 2 activation by bacterial peptidoglycan–associated lipoprotein activates cardiomyocyte inflammation and contractile dysfunction

Abstract

Our data reveal that PAL uses the TLR2/MyD88 signaling cascade to induce cardiomyocyte dysfunction and inflammatory responses and that TNFalpha is a major mediator of PAL-induced dysfunction in cardiomyocytes. These studies suggest that circulating PAL and other TLR2 agonists may contribute to cardiac dysfunction in sepsis.