The Journal of surgical research
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Pseudomonas aeruginosa causes serious infections in severely burned patients due to its ability to produce numerous virulence factors. The production of most of these factors is controlled by the cell-to-cell communication system called quorum sensing (QS). We have recently shown that several proinflammatory and hematopoietic cytokines are produced during infection of the burn wound with P. aeruginosa strain PAO1. Most of these cytokines were not produced during either thermal injury or P. aeruginosa infection alone. ⋯ These results suggest that: 1) the QS system is involved in the induction of cytokine expression during P. aeruginosa infection of burn wounds; and 2) this effect may be caused by either a component of the QS system or a QS-controlled virulence factor.
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Studies indicate that following septic insult there is development of generalized immune dysfunction in T cells, B cells and phagocytes, which is thought to contribute to morbidity and mortality. Specifically, there is a shift in the lymphocytes of septic animals toward an increased release of Th2 cytokines. NK-T cells have been shown to contribute to propagation of the Th2 response. The influence of NK-T cells on the immune response to septic challenge is poorly understood. In this study, we examine whether NK-T cells contribute to the immune dysfunction seen following the onset of polymicrobial sepsis, as produced by cecal ligation and puncture (CLP). ⋯ Together these findings imply not only that NK-T cells may play a role in mediating the immune suppression seen in bacterial sepsis, but that inhibition of their activation promotes survival to septic challenge.
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Gut ischemia/reperfusion (I/R) elicits an inflammatory response that impairs intestinal transit. We have previously shown that regional intraischemic hypothermia (IH) protects against moderate gut I/R-induced mucosal injury, is associated with decreased NF-kappaB activity and inducible nitric oxide synthase induction and preserves heme oxygenase-1 (HO-1) expression. HO-1 provides cytoprotection in various models of oxidant stress. We, therefore, tested the hypothesis that IH protects against gut I/R-induced impaired intestinal transit via HO-1 induction. ⋯ We conclude that intraischemic regional hypothermia protects against histological injury and impaired intestinal transit caused by severe gut I/R injury. Hypothermic protection under these conditions is in part due to HO-1 expression.
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Body-composition changes have been observed after burn injury. In particular, several studies have shown that bone mineral density (BMD) in burn patients is decreased when compared to the normal population. Little is known about the frequency, severity, or duration of these changes. The purpose of this study was to describe body-composition changes over time after burn injury. ⋯ These results confirm earlier studies, suggesting that BMD can be negatively altered post-injury, with the greatest changes occurring after patients are discharged from the hospital. Although the clinical significance of these changes is not known, this study supports the need for long-term musculoskeletal assessments in burn patients and for further research to elucidate the mechanisms of burn-induced body-composition changes.
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During hemorrhagic shock blood flow to vital organs is maintained by the diversion of blood from both the splanchnic organs and skeletal muscle. In this swine study, we tested the hypotheses that (1). liver and muscle pH are correlated during both shock and resuscitation and (2). muscle pH during shock is an indicator of potential liver injury after resuscitation. ⋯ Minimally invasive measurement of muscle pH warrants further study as a method to assess splanchnic hypoperfusion and resultant injury.