Key result
Septic plasma activates cardiac myocytes via TNF-alpha and IL-1beta, which subsequently promote neutrophil transendothelial migration through the release of CXC chemokines LIX and KC.
Population
Cardiac myocytes isolated from rats with peritonitis and plasma from mice subjected to cecal ligation and…
Design
Preclinical
Authors
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Hypothesis-generating for cytokine blockade in sepsis cardiomyopathy; leaves open translation from rodent models to patients.
This study identifies the mechanistic pathways by which sepsis-induced circulating factors activate cardiac myocytes to promote neutrophil infiltration, highlighting potential therapeutic targets for sepsis-induced cardiac inflammation.
Madorin et al. (2004) studied Peritonitis / Sepsis. Septic plasma was evaluated on PMN transendothelial migration and myocyte activation. Septic plasma activates cardiac myocytes via TNF-alpha and IL-1beta, which subsequently promote neutrophil transendothelial migration through the release of CXC chemokines LIX and KC.
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