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CHARACTERIZATION OF THE INFLAMMATORY RESPONSE DURING ACUTE AND POST-ACUTE PHASES AFTER SEVERE BURN
Open accessAbstract
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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“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]
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Self-citation
Metadata
- 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)
- PMC
- PMC7863568
- 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
- green
- europepmc.org
- 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 › Surgery › Burn Injury Management and Outcomes
- Health Sciences › Medicine › Surgery › 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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