title: Characterization of the inflammatory response during acute and post-acute phases after severe burn.
abstract: Severe burn causes a pronounced hypermetabolic response characterized by catabolism and extensive protein wasting. We recently found that this hypermetabolic state is driven by a severe inflammatory response. We characterized in detail the kinetics of serum levels of a panel of cytokines in a rat model, which may serve as reference for the development of therapeutic interventions applicable to humans. Male Sprague-Dawley rats (n = 8) received a full-thickness burn of 60% total body surface area. Serum was harvested 1, 3, 6, 12, 24, 48, 96, and 168 h after burn. Eight serum cytokines commonly used to assess the inflammatory response in humans, such as IL-1beta, IL-6, IL-10, TNF, vascular endothelial growth factor, and monocyte chemotactic protein 1, and the rat-specific cytokines cytokine-induced neutrophil chemoattractant (CINC) 1, CINC-2, and CINC-3 were measured by enzyme-linked immunosorbent assay technique and were compared with controls (n = 4). Statistical analysis was conducted using the t test, with P < 0.05 considered as significantly different. Thermal injury resulted in significantly increased serum levels of IL-1beta, IL-6, IL-10, monocyte chemotactic protein 1, CINC-1, CINC-2, and CINC-3 when compared with the concentrations detected in nonburned rats (P < 0.05). Serum levels of TNF-alpha and vascular endothelial growth factor in burned rats were not found to be significantly different to controls. Burn causes a profound inflammatory response in rats. Specific cytokines known to increase in humans postburn such as IL-1 beta, IL-6, IL-10, MCP-1, and IL-8 (CINC-1, CINC-2, and CINC-3 in the rat) were also observed in our rat burn model, which now allows us to study new anti-inflammatory treatment options.
authors.affiliation: Shriners Hospital for Children, Galveston, Texas 77550, USA.
authors.forename: Gerd G
authors.initials: GG
authors.lastname: Gauglitz
authors.forename: Juquan
authors.initials: J
authors.lastname: Song
authors.forename: David N
authors.initials: DN
authors.lastname: Herndon
authors.forename: Celeste C
authors.initials: CC
authors.lastname: Finnerty
authors.forename: Darren
authors.initials: D
authors.lastname: Boehning
authors.forename: José M
authors.initials: JM
authors.lastname: Barral
authors.forename: Marc G
authors.initials: MG
authors.lastname: Jeschke
mesh_terms: D000818:Animals; D002056:Burns / Q000097:blood* / Q000276:immunology* / Q000503:physiopathology; D018932:Chemokine CCL2 / Q000097:blood; D054360:Chemokine CXCL1 / Q000097:blood; D019743:Chemokines, CXC / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D007249:Inflammation / Q000097:blood* / Q000276:immunology*; D007375:Interleukin-1 / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D018932:Chemokine CCL2; D054360:Chemokine CXCL1; D019743:Chemokines, CXC; C513297:Cxcl1 protein, rat; C513294:Cxcl3 protein, rat; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D016753:Interleukin-10