Abstract
Age‐related changes in wound healing have been characterized by alterations in the early inflammatory, proliferative and late remodeling phases. Aging has also been associated with decline of the innate and adaptive immune response, contributing to morbidity and mortality following infection. This study will characterize the effect of advanced age on the inflammatory response to full‐thickness dermal injury in a murine model. In response to injury, aged mice exhibited decreased neutrophil infiltration into the wound as compared to young mice. Further, macrophage inflammatory protein‐2 (MIP‐2) levels remained elevated in aged mice 72 hours post injury, whereas the levels of this chemokine decrease in young mice after 48 hours. Additionally, the dendritic cell population was decreased by 65% in uninjured aged skin. Interestingly, after injury, the dendritic cell population decreased in young mice and increased in aged mice. These data suggest an age‐related differential response to dermal wound healing that may impact the innate immune response to infectious challenge.Grant Funding Source: National Institute of Health R01 AG506080 (EJK) and the Ralph and Marian C Falk Medical Research Trust
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