Journal article
Elevated monocyte chemoattractant protein‐1 levels following thermal injury precede monocyte recruitment to the wound site and are controlled, in part, by tumor necrosis factor‐α
Wound repair and regeneration, Vol.11(2), pp.110-119
03/2003
DOI: 10.1046/j.1524-475X.2003.11206.x
PMID: 12631298
Abstract
In previous studies, mice given a full-thickness scald injury had an influx of neutrophils into the skin that followed a local increase in a neutrophil chemoattractant. Because macrophages are known to infiltrate the wound area after neutrophils and are essential for normal wound repair, studies were designed to characterize the time course of macrophage accumulation in the wound and to identify the factor(s) responsible for this influx. A macrophage infiltrate into the wound was observed at 4 days post-injury and persisted through at least 10 days. This influx was preceded by an initial fourfold increase in dermal monocyte chemoattractant protein-1 levels at 24 hours post-injury (p < 0.05). This elevation in monocyte chemoattractant protein-1 was enhanced at 4 and 10 days postburn resulting in a sixfold increase over baseline (p < 0.01). Levels of tumor necrosis factor-alpha, a proinflammatory cytokine known to induce chemokine production, were elevated at 90 minutes after injury in burn- versus sham-injured groups (p < 0.05). Furthermore, administration of tumor necrosis factor-alpha neutralizing antibody in vivo reduced the dermal levels of monocyte chemoattractant protein-1 seen at 10 days postburn by 57% (p < 0.01); however, macrophage accumulation was not altered. Thus, elevated systemic TNF-alpha levels may influence the local chemokine milieu following burn injury.
Details
- Title: Subtitle
- Elevated monocyte chemoattractant protein‐1 levels following thermal injury precede monocyte recruitment to the wound site and are controlled, in part, by tumor necrosis factor‐α
- Creators
- Scott A Heinrich - From the Department of Cell Biology, Neurobiology and Anatomya;, Burn and Shock Trauma InstitutebKelly A. N Messingham - From the Department of Cell Biology, Neurobiology and Anatomya;, Burn and Shock Trauma Instituteb;, Alcohol Research Programg, Loyola University Medical Center, Maywood, IllinoisMeredith S Gregory - From the Department of Cell Biology, Neurobiology and Anatomya;, Burn and Shock Trauma InstitutebAlessandra Colantoni - Burn and Shock Trauma Instituteb;, Department of Surgeryd;, Division of Gastroenterology/Department of Medicinee;, Aging and Immunology Programf;, Alcohol Research Programg, Loyola University Medical Center, Maywood, IllinoisAhalia M Ferreira - Burn and Shock Trauma InstitutebLuisa A Dipietro - Burn and Shock Trauma Instituteb;, Department of Microbiology and Immunologyc;, Aging and Immunology ProgramfElizabeth J Kovacs - From the Department of Cell Biology, Neurobiology and Anatomya;, Burn and Shock Trauma Instituteb;, Department of Surgeryd;, Aging and Immunology Programf;, Alcohol Research Programg, Loyola University Medical Center, Maywood, Illinois
- Resource Type
- Journal article
- Publication Details
- Wound repair and regeneration, Vol.11(2), pp.110-119
- DOI
- 10.1046/j.1524-475X.2003.11206.x
- PMID
- 12631298
- ISSN
- 1067-1927
- eISSN
- 1524-475X
- Language
- English
- Date published
- 03/2003
- Academic Unit
- Dermatology
- Record Identifier
- 9984025325402771
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