Myocardial Inflammatory Responses to Sepsis Complicated by Previous Burn Injury

Abstract

A previous burn injury alters myocardial inflammatory responses, predisposing the burn-injured subject to exaggerated inflammation, which correlates with greater myocardial dysfunction.

Effect of Aspiration Pneumonia-Induced Sepsis on Post-Burn Cardiac Inflammation and Function in Mice

“…Our experimental studies have confirmed that burn injury in rats alters immune function such that a second insult, such as a gram-positive or gram-negative infection, increases the morbidity and mortality over that observed with either burn alone or infection alone [12][13][14]. Recent availability of genetically engineered animals with either overexpression or deletion of selected genes stimulated our interest in mouse models of burn injury, sepsis, or burn complicated on post-burn day seven by aspiration pneumonia-induced sepsis.…”

Reducing susceptibility to bacteremia after experimental burn injury: a role for selective decontamination of the digestive tract

“…While we considered that SDD may have reduced sensitivity to a subsequent infectious challenge, we also considered that bacterial killing was increased as a direct antibiotic effect of SDD therapy or by an indirect mechanism that preserved innate killing mechanisms. In our study, SDD therapy decreased both plasma and cardiac myocyte-secreted inflammatory cytokine levels; this reduced inflammatory response was paralleled by improved cardiac performance in SDD-treated animals, and these data are consistent with previous reports that inflammatory cytokines are primary mediators of postburn myocardial contraction and relaxation defects (12,13). In our study, the SDD-related decrease in IL-10 response was attributed to the SDD-mediated attenuation of inflammatory responses and a decrease in compensatory anti-inflammatory responses.…”

“…We confirmed that Ͻ2% of the total cell number in a myocyte preparation was noncardiomyocytes. Since our preparations are 98% cardiomyocytes, we concluded that a majority of the inflammatory cytokines measured in the cardiomyocyte supernatants was indeed cardiomyocyte derived (12).…”

Platelet-Activating Factor Receptor and Innate Immunity: Uptake of Gram-Positive Bacterial Cell Wall into Host Cells and Cell-Specific Pathophysiology

“…Initiation of antibiotic therapy in the context of sepsis rapidly releases cell wall fragments in the bloodstream, an effect that is well known to correlate with transient impairment of cardiac function (65)(66)(67). Such detrimental effects of cell wall uptake on cardiac physiology were demonstrable in the mouse model both in terms of survival and cardiac dysfunction.…”