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Permissive environment in postnatal wounds induced by adenoviral‐mediated overexpression of the anti‐inflammatory cytokine interleukin‐10 prevents scar formation
Author(s) -
Gordon Ashley,
Kozin Elliott D.,
Keswani Sundeep G.,
Vaikunth Sachin S.,
Katz Anna B.,
Zoltick Philip W.,
Favata Michele,
Radu Antoneta P.,
Soslowsky Louis J.,
Herlyn Meenhard,
Crombleholme Timothy M.
Publication year - 2007
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1524-475x.2007.00326.x
Subject(s) - wound healing , inflammation , fetus , cytokine , permissive , medicine , extracellular matrix , gestation , interleukin , pathology , immunology , biology , microbiology and biotechnology , pregnancy , genetics , virology
Wound healing in the mid‐gestation fetus is scarless with minimal inflammation and a unique extracellular matrix. We have previously documented the relative lack of inflammatory cytokines in this environment. We demonstrate that interleukin (IL)‐10 is highly expressed in mid‐gestation human fetal skin but is absent in postnatal human skin. We hypothesize that overexpression of IL‐10 in postnatal skin may replicate a permissive environment for scarless healing. To study the mechanism underlying this process we performed immunohistochemistry for IL‐10 in human mid‐gestation fetal and postnatal skin. We also determined if adenoviral‐mediated overexpression of IL‐10 could allow for scarless wound healing in a murine incisional wound model. Wounds were analyzed at 1–90 days postwounding for effects on scar formation, inflammatory response, and biomechanical properties. Ad‐IL‐10 reconstitutes a permissive environment for scarless healing as shown by reconstitution of a normal dermal reticular collagen pattern and distribution of dermal elements. Compared with controls, Ad‐IL‐10 treated wounds showed reduced inflammatory response and no difference in biomechanical parameters. Therefore, overexpression of IL‐10 in postnatal wounds results in a permissive environment for scarless wound repair, possibly by replicating a fetal wound environment.