Cited by 142Burn Injury Management and OutcomesWound Healing and TreatmentsInflammation biomarkers and pathways

Characterization of the inflammatory response during acute and post-acute phases after severe burn

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Gauglitz, Gerd G., Song, Juquan, Herndon, David N., Finnerty, Celeste C., Boehning, Darren, Barral, José M., Jeschke, Marc G.·2008·Shock

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.

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Crossref · 10.1097/shk.0b013e31816e3373

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  • MMP2 and 9 levels are elevated very early and reduced at later time points in wound tissue of THS-exposed mice.

    “The levels of MMP2 and 9 which are very important in reepithelization and tissue remodelling [31,32], are elevated very early on and reduced at later time points in the wound tissue of THS-expose mice suggesting its role in impaired wound closure.”

    From Tobacco toxins deposited on surfaces (third hand smoke) impair wound healing (2016) · cites this paper as [31]

    The citation is attached to the statement that MMP2 and MMP9 are important in reepithelialization and tissue remodeling; the THS-exposed mouse finding appears to be the citing authors’ own result. The cited paper’s Methods and Results describe serum cytokines in burned rats, not the proposed roles of MMP2 or MMP9. Searches for MMP2, MMP9, reepithelialization, and tissue remodeling found no passage addressing that attributed point. (LLM, conf=0.75)

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Research works printed but not linked: 2

  1. [9]Herndon DN: Total Burn Care. New York, NY: WB Saunders, 2002.
  2. [25]Vindenes H, Ulvestad E, Bjerknes R: Increased levels of circulating interleukin-8 in patients with large burns: relation to burn size and sepsis. J Trauma 39(4): 635– 640, 1995. 7473946

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Authors
Gauglitz, G. G., Song, J., Herndon, D. N., Finnerty, C. C., Boehning, D., Barral, J. M., & Jeschke, M. G.
Affiliations
  • Shriners Hospitals for Children - Galveston (US)
  • Shriners Hospitals for Children (US)
  • The University of Texas Medical Branch at Galveston (US)
Corresponding author
  • Gauglitz, Gerd G.
  • Song, Juquan
  • Herndon, David N.
  • Finnerty, Celeste C.
  • Jeschke, Marc G.
Venue
Shock
Published
2008-11
Volume
30
Issue
5
Pages
503-507
ISSN
1073-2322 (ISSN-L)
OpenAlex
W1981192549
Cited by
142
References
46
Citations by year
2026: 5 · 2025: 5 · 2024: 3 · 2023: 7 · 2022: 12 · 2021: 6 · 2020: 10 · 2019: 7 · 2018: 6 · 2017: 8 · 2016: 5 · 2015: 12 · 2014: 9 · 2013: 4 · 2012: 8
FWCI
8.44
Type
journal article
Language
en
Open access
Locations
  • Shock (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of General Medical Sciences (P50GM060338, R01 GM 56687, R01GM056687, P50 GM-60338, T32GM008256)
Topics
  • Health Sciences › Medicine › Epidemiology › Burn Injury Management and Outcomes
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
severe burns, inflammation, cytokines, hypermetabolism, third-degree burns, IL-1β, interleukin-6, IL-10, MCP-1, CINC-1, TNF-α, vascular endothelial growth factor, rat burn model, anti-inflammatory therapy
MeSH terms
Animals, Burns, Enzyme-Linked Immunosorbent Assay, Inflammation, Interleukin-1, Male, Tumor Necrosis Factor-alpha, Interleukin-6, Interleukin-8, Interleukin-10, Rats, Sprague-Dawley, Chemokine CCL2, Chemokines, CXC, Vascular Endothelial Growth Factor A, Rats, Chemokine CXCL1

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