Abstract
This study tested the hypothesis that xenogeneic human umbilical cord-derived mesenchymal stem cell (HUCDMSC) therapy would improve survival rates in rats with acute respiratory distress-syndrome (ARDS, induction by 48 h inhalation of 100% oxygen) and sepsis-syndrome (SS, induction by cecal-ligation and puncture) (ARDS-SS). Adult-male Sprague-Dawley rats were categorized into group 1 (sham-controls), group 2 (ARDS-SS), group 3 [ARDS-SS+HUCDMSC (1.2 ×106 cells administered 1 h after SS-induction)], and group 4 [ARDS-SS+HUCDMSC (1.2 ×106 cells administered 24 h after SS-induction)]. The mortality rate was higher in groups 2 and 4 than in groups 1 and 3 (all p<0.0001). The blood pressure after 28 h was lower in groups 2, 3 and 4 (p<0.0001) than in group 1. Albumin levels and percentages of inflammatory cells in broncho-alveolar lavage fluid, and the percentages of inflammatory and immune cells in circulation, were lowest in group 1, highest in group 2, and higher in group 3 than group 4 (all p<0.0001). The percentages of inflammatory cells in ascites and kidney parenchyma showed identical patterns, as did kidney injury scores (all p<0.0001). EarlyHUCDMSC therapy reduced rodent mortality after induced ARDS-SS.
Highlights
Acute respiratory distress syndrome (ARDS) and sepsis syndrome with multiple organ failure (SS) are two global, growing diseases that have high in-hospital mortality [1,2,3,4,5]
This study investigated the impact of human umbilical cord-derived mesenchymal stem cell (HUCDMSC) therapy on the prognostic outcome in rats after inducing ARDS-SS
ARDS-SS induction was always followed by an elevated inflammatory reaction, while HUCDMSC treatment suppressed it
Summary
Acute respiratory distress syndrome (ARDS) and sepsis syndrome with multiple organ failure (SS) are two global, growing diseases that have high in-hospital mortality [1,2,3,4,5]. Patients with both ARDS and SS (ARDS-SS) experience an uncontrolled immune response, inflammation, over-production of reactive oxygen species (ROS), over-activation (i.e., cascade) of complement, and endotoxin release from infectious microorganisms [4, 10, 13,14,15,16,17,18,19,20,21,22,23,24] These complex hyper-inflammatory and immune responses are triggered in an attempt to eliminate the causative factors, but they cause multi-organ damage in the host [17, 20], which could contribute to the high mortality in ARDS-SS [13,14,15,16,17,18,19,20,21,22,23,24]. Strategies that target these increased inflammatory and immune responses may have therapeutic potential
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