Burn wounds infected with Pseudomonas aeruginosa triggers weight loss in rats

被引：7
作者：
Steinstraesser L. [1 ,2 ]
Burkhard O. [1 ,4 ]
Fan M.H. [1 ]
Jacobsen F. [4 ]
Lehnhardt M. [4 ]
Su G. [2 ]
Daigler A. [4 ]
Steinau H.U. [4 ]
Remick D. [3 ]
Wang S.C. [1 ]
机构：
[1] Dept. of Surgery, University of Michigan, Ann Arbor, MI 48109-0666
[2] Medicine, University of Michigan, Ann Arbor, MI 48109-0666
[3] Pathology, University of Michigan, Ann Arbor, MI 48109-0666
[4] Dept. Plastic Surgery Burn Center, Ruhr-University Bochum, 44789 Bochum
来源：
BMC Surgery | / 5卷 / 1期
关键词：
Infected Group; Thermal Injury; Endotoxin Level; Total Body Surface Area; Treatment Control Group;
D O I：
10.1186/1471-2482-5-19
中图分类号：
学科分类号：
摘要：
Background: Despite dramatic improvements in the management of burns, infection still remains a serious risk for the burn patient. The aim of this study was to shed light on the impact of acute burn injury with or without infection on cytokine profiles. Methods: Sprague-Dawley rats (n = 21) were randomized into three groups: 1) burn only 2) burn and infection or 3) sham burn. Weight was monitored and blood was collected for cytokine ELISA, LPS quantification, and peripheral blood analysis. Animals were sacrificed either after 6 or 12 days. Results: Infected animals showed substantial weight loss until day 6 post-burn as compared to burn alone. Endotoxin and TNF-α levels were elevated early in the infected burn group within 48 hours post-burn. In contrast, significant up-regulation of the anti-inflammatory cytokine IL-10 occurred later in the clinical course and was associated with the recovery from weight loss. Conclusion: Our results suggest that in the presence of infection, you get a SIRS response possibly due to transient endotoxemia that is only seen in the infection group. In contrast, both burn and infection get a late IL-10 (CARS) response, which is then associated with a return to normal weight in the infection group. © 2005 Steinstraesser et al; licensee BioMed Central Ltd.
引用
收藏
相关论文
共 36 条
  • [1] Baue A.E., Durham R., Faist E., Systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), multiple organ failure (MOF): Are we winning the battle?, Shock, 10, 2, pp. 79-89, (1998)
  • [2] Harris B.H., Gelfand J.A., The immune response to trauma, Semin Pediatr Surg, 4, 2, pp. 77-82, (1995)
  • [3] Nguyen T.T., Gilpin D.A., Meyer N.A., Herndon D.N., Current treatment of severely burned patients, Ann Surg, 223, 1, pp. 14-25, (1996)
  • [4] Saffle J.R., Sullivan J.J., Tuohig G.M., Larson C.M., Multiple organ failure in patients with thermal injury, Crit Care Med, 21, 11, pp. 1673-1683, (1993)
  • [5] Still J.M.J., Belcher K., Law E.J., Experience with polymicrobial sepsis in a regional burn unit, Burns, 19, 5, pp. 434-436, (1993)
  • [6] Teodorczyk-Injeyan J.A., Sparkes B.G., Mills G.B., Peters W.J., Falk R.E., Impairment of T cell activation in burn patients: A possible mechanism of thermal injury-induced immunosuppression, Clin Exp Immunol, 65, 3, pp. 570-581, (1986)
  • [7] Steinstraesser L., Oezdogan Y., Wang S.C., Steinau H.U., Host defense peptides in burns, Burns, 30, 7, pp. 619-627, (2004)
  • [8] Nizet V., Ohtake T., Lauth X., Trowbridge J., Rudisill J., Dorschner R.A., Pestonjamasp V., Piraino J., Huttner K., Gallo R.L., Innate antimicrobial peptide protects the skin from invasive bacterial infection, Nature, 414, 6862, pp. 454-457, (2001)
  • [9] Meakins J.L., Etiology of multiple organ failure, J Trauma, 30, 12 SUPPL., (1990)
  • [10] Hengge U.R., Benninghoff B., Ruzicka T., Goos M., Topical immunomodulators - Progress towards treating inflammation, infection, and cancer, Lancet Infect Dis, 1, 3, pp. 189-198, (2001)
1234