• Sam Jacob, Yong Zhu, Robert Kraft, Christopher Cotto, Joseph R Carmical, Thomas G Wood, Perenlei Enkhbaatar, David N Herndon, Hal K Hawkins, and Robert A Cox.
• Departmentof Pathology, Shriners Hospitals for Children and The University of Texas Medical Branch Galveston, Texas, USA.
• Int J Burns Trauma. 2015 Jan 1; 5 (1): 36-45.

AbstractPneumonia is the leading complication in the critical care of burn victims. Airway epithelial dysfunction compromises host defense against pneumonia. The aim of this study is to test the hypothesis that burn injury alters the physiology of the airway epithelium. A rat model of 60% TBSA third degree scald burn was used. At 24 hours after injury, tracheal epithelial ultrastructure was studied using transmission electron microscopy (TEM) and proliferation was measured by Ki67 immunohistochemistry. Mucociliary clearance (MCC) was measured using fluorescent microspheres. The level of malondialdehyde (MDA), an indicator of lipid peroxidation, was also measured. Changes in epithelial mRNA expression were measured using microarray. Burn injury led to a ten-fold reduction in MCC that was statistically significant (p = 0.007) 24 hours after injury. No significant change was noted in the morphology of tracheal epithelial cells between groups, although a marginal increase in extracellular space was noted in injured animals. Ki67 nuclear expression was significantly reduced (25%, p = 0.008) in injured rats. There was a significant increase in MDA levels in the epithelial lysate of burned animals, p = 0.001. Microarray analysis identified 59 genes with significant differences between sham and injured animals. Burn injury altered multiple important functions in rat tracheal epithelium. The decrease in MCC and cell proliferation may be due to oxidative injury. Mechanistic studies to identify physiological processes associated with changes in airway function may help in designing therapeutic agents to reduce burn-induced airway pathogenesis.

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