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Aging
Alters the Inflammatory and Endothelial Cell Adhesion Molecule Profiles
during Human Cutaneous Wound Healing |
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Gillian S.
Ashcroft, Michael A. Horan, and Mark W. J. Ferguson |
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School
of Biological Sciences (GSA, MWJF), University of Manchester, and University
Department of Geriatric Medicine (GSA, MAH), Hope Hospital, Salford, Manchester,
United Kingdom |
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Age-related changes in
the human inflammatory response in vivo have been largely ignored, resulting
in a lack of understanding of the patho-physiologic processes involving
inflammation that become increasingly important with age, of which wound
repair is an important example. We have tested the hypothesis that the delay
in wound healing resulting from old age is associated with an altered inflammatory
response and endothelial cell adhesion molecule (CAM) profile, because CAMs
influence the temporal and lineage profiles of extravasated leukocytes within
a wound. Cutaneous punch biopsies were taken from 138 healthy subjects,
aged 19 to 96 years; the wounds were rebiopsied at fixed time-points from
Day 1 up to 3 months postwounding. Quantitative image analysis showed that
there was a marked early increase in the neutrophil response in the aged
with a less pronounced peak in the wounds of young subjects. Monocyte/macrophage
and lymphocyte appearance was delayed in the aged with cell numbers peaking
at Day 84, compared to Day 7 for monocytes and Day 21 for lymphocytes in
the young, but with increased numbers of mature macrophages in the aged.
E-selectin was strongly expressed in a perivascular distribution in the
early wounds of the aged; however, only faint staining was seen from Day
3 to 7 in the wounds of the young. Intracellular CAM-1 and vascular CAM-1
expression exhibited an age-related delay in appearance and a reduction
in staining intensity. This altered CAM profile may affect the early inflammatory
wound healing response in aged humans and suggests a target for future therapeutic
manipulations. |
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