In order to determine the mechanism(s) for the adverse LV remodeling in the Dysf−/− mouse hearts, we backcrossed Dysf−/− mice with mice lacking the Toll-Interleukin 1 Receptor (TIR) Domain-Containing Adaptor Protein (TIRAP), which is involved in bridging the myeloid differentiation primary response gene 88 (MyD88) to the receptor complex for TLR2 and TLR4 signaling in response to bacterial infection or tissue injury, in order to generate Dysf−/−/Tirap−/− double knock out mice. This evidence concerns the gene TLR2 and bacterial infectious disease.