Cytokine and chemokine release upon prolonged mechanical loading of the epidermis

: At this moment, pressure ulcer risk assessment is dominated by subjective measures and does not predict pressure ulcer development satisfactorily. Objective measures are, therefore, needed for an early detection of these ulcers. The current in vitro study evaluates cytokines and chemokines [inter...

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Bibliographic Details
Published in:	Experimental dermatology Vol. 16; no. 7; pp. 567 - 573
Main Authors:	Bronneberg, Debbie, Spiekstra, Sander W., Cornelissen, Lisette H., Oomens, Cees W. J., Gibbs, Susan, Baaijens, Frank P. T., Bouten, Catlijin V. C.
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-07-2007 Blackwell
Subjects:	Biological and medical sciences Biomarkers Cells, Cultured Chemokines - biosynthesis Cytokines - biosynthesis Dermatology EpiDerm Epidermis - metabolism Epidermis - pathology Humans interleukin 1 receptor antagonist Interleukin 1 Receptor Antagonist Protein - biosynthesis interleukin 1α interleukin 8 Interleukin-1alpha - biosynthesis Interleukin-8 - biosynthesis Medical sciences Models, Biological Pressure - adverse effects pressure ulcer Pressure Ulcer - etiology Pressure Ulcer - metabolism Skin involvement in other diseases. Miscellaneous. General aspects Stress, Mechanical tumor necrosis factor α Tumor Necrosis Factor-alpha - biosynthesis Skin disease Angiogenic factor Dermatology Interleukin 1 receptor antagonist Cytokine Epidermis Pressure sore EpiDerm pressure ulcer Chemokine tumor necrosis factor a interleukin la Mechanical load Tumor necrosis factor α Interleukin 8 Release Prolonged
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Summary:	: At this moment, pressure ulcer risk assessment is dominated by subjective measures and does not predict pressure ulcer development satisfactorily. Objective measures are, therefore, needed for an early detection of these ulcers. The current in vitro study evaluates cytokines and chemokines [interleukin 1α (IL‐1α), interleukin 1 receptor antagonist (IL‐1RA), tumor necrosis factor α (TNF‐α) and interleukin 8 (CXCL8/IL‐8)] as early markers for mechanically‐induced epidermal damage. Various degrees of epidermal damage were induced by subjecting commercially available epidermal equivalents (EpiDerm) to increasing pressures (0, 50, 75, 100, 150, and 200 mmHg) for 24 h, using a loading device. At the end of the loading experiment, tissue damage was assessed by histological examination and by evaluation of the cell membrane integrity. Cytokines and chemokines were determined in the culture supernatant. Sustained epidermal loading resulted in an increased release of IL‐1α, IL‐1RA, TNF‐α and CXCL8/IL‐8. This was first observed at 75 mmHg, when the tissue was only slightly damaged. Swollen cells, vacuoles, necrosis and affected cell membranes were observed at pressures higher than 75 mmHg. Furthermore, at 150 and 200 mmHg, the cells in the lower part of the epidermis were severely compressed. In conclusion, IL‐1α, IL‐1RA, TNF‐α and CXCL8/IL‐8 are released in vitro as a result of sustained mechanical loading of the epidermis. The first increase in cytokines and chemokines was observed when the epidermal tissue was only slightly damaged. Therefore, these cytokines and chemokines are potential markers for the objective, early detection of mechanically‐induced skin damage, such as pressure ulcers.
Bibliography:	istex:6867B1A3BE9D61D98A0CD18B929454BED9DA2C58 ark:/67375/WNG-GGTXMQCV-M ArticleID:EXD566 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0906-6705 1600-0625
DOI:	10.1111/j.1600-0625.2007.00566.x