Signs of persistent neuroinflammation after myocardial infarction of mice (730.3)

Acute myocardial infarction (MI) evokes production of circulating pro‐inflammatory cytokines, which can result in neuroinflammation. This study aimed to investigate signs of neuroinflammation in mice by measuring brain TNF‐alpha expression and microglia activation after MI. Male 14 week old C57 Bl/6 mice were subjected to MI or sham surgery. Two weeks later, infarct was verified by ECHO‐cardiography, and mice were sacrificed. Brain was processed for western blot on TNF‐alpha, and TNF‐receptors. Heart failure in MI mice was confirmed by increased lung dry weight (35.2±2.2 vs 30.1±0.7 mg), and reduced fractional shortening (19±3 vs 46±1%). TNF‐alpha precursor expression was significantly increased in MI versus sham (9.79±0.60 vs 6.99±0.64 AU) and was associated with higher TNF‐R1 (5.92±2.39 vs 1.88±0.36 AU) and lower TNF‐R2 expression (0.71±0.61 vs 3.01±0.95 AU). Brain tissue stained for microglia showed increased numbers of microglia in the dentate gyrus of the hippocampus (17.1±0.8 vs 14.7±0.8 per high power field) combined with a decreased ratio of processes/cell body surface area (0.071±0.004 vs 0.098±0.007), indicating a higher degree of activation. MI in mice induces increased TNF‐alpha expression at higher TNF‐R1 and lower TNF‐R2 expression in the brain, indicating a persistent pro‐inflammatory state. Spatially altered number of microglia may suggest localization of this inflammation.