Wound healing is a complex cellular and molecular event during the inflammatory phase after injury. Infiltrating and resident cells interact to decontaminate and debride the wound promoting re-epithelialization of wound surfaces. Cytokines and growth factors are important mediators of inflammation and repair in this environment. This study proposes to evaluate potential mechanisms relating neuroendocrine responses, cytokine gene expression, and wound healing utilizing a murine model of restrained stress. The hypothesis specifically states that restrained stress will delay wound healing by depressing the early inflammatory response which is reflected by down regulation of proinflammatory cytokines IL-La, IL-1b and TNFa and impact on keratinocyte growth factor which is critical for re-epithelialization of the wound.
Three specific aims are proposed.
The first aim characterizes the proinflammatory cytokine and KGF mRNA in excised wounds and blood of control vs. restrained mice.
The second aim characterizes the cellular localization of this message in the wounds, and the third aim determines the relationship between plasma corticosterone levels and the expression of cytokine and growth factor message in excised wounds in the restrained mouse model.
| Mercado, Ana M; Quan, Ning; Padgett, David A et al. (2002) Restraint stress alters the expression of interleukin-1 and keratinocyte growth factor at the wound site: an in situ hybridization study. J Neuroimmunol 129:74-83 |
| Mercado, Ana M; Padgett, David A; Sheridan, John F et al. (2002) Altered kinetics of IL-1 alpha, IL-1 beta, and KGF-1 gene expression in early wounds of restrained mice. Brain Behav Immun 16:150-62 |
