• Juquan Song, Steven E Wolf, David N Herndon, Xiao-Wu Wu, and Marc G Jeschke.
• Shriners Hospitals for Children and Department of Surgery, the University of Texas Medical Branch, Galveston, TX 77550, USA.
• Shock. 2008 Aug 1; 30 (2): 184-8.

AbstractSecondary infections after burn are common and are a major contributor to morbidity and mortality. We previously showed that burn disrupted proximal gut mucosal homeostasis through increased epithelial cell apoptosis. In the present study, we sought to determine whether proximal gut mucosal disruption is additively affected by secondary endotoxemia after a severe burn. C57BL/6 mice received 30% total body surface area full-thickness scald burns and were randomized to receive saline or LPS 1 mg/kg body weight given intraperitoneally 72 h after burn. Proximal small bowel was harvested 12 h after LPS injection. Mucosal height and epithelial cell number were assessed on hematoxylin-eosin sections, intestinal epithelial cell apoptosis was identified by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and cell proliferation by immunohistochemical staining for proliferating cell nuclear antigen. Results showed that proximal gut mucosa impairment occurred 12 h after injury, including significantly decreased proximal gut wet weight, gut mucosal height, and epithelial cell number associated with increased proximal gut epithelial apoptosis (P < 0.05). This impairment diminished 72 h after burn. Second-hit endotoxemia caused additional proximal gut mucosa damage with decreased proximal gut weight, cell number, and mucosal height (P < 0.05) and significantly increased small intestinal epithelial apoptosis and mucosal atrophy, even after the first event, indicating a second detrimental effect of endotoxemia after the initial injury.

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