Important role of p38 MAP kinase/NF-KB signaling pathway in the sepsis-induced conversion of cardiac myocytes to a proinflammatory phenotype

摘要

Neutrophil infiltration of the myocardium would be facilitated by the generation of a chemotactic gradient by resident interstitial cells. Immune cells (e.g., macrophages) are generally considered as major sources of the primary inflammatory mediators with chemotactic potential (26). We have recently provided evidence indicating that cardiac myocytes, per se, can play an important role in PMN infiltration of the heart (22). Exposure of isolated cardiac myocytes to plasma from septic animals converted them to a proinflammatory phenotype; these myocytes produced CXC chemokines, KC and L1X, and promoted PMN transendothelial migration. The conversion of cardiac myocytes to a proinflammatory phenotype was attributed to activation and nuclear translocation of the transcription factor nuclear factor-KB (NF-kB).