Wound Healing

Critical for efficient wound healing is an appropriate inflammatory response, which i s characterised in part by infiltration into the wound of neutrophils and macrophages. Upon arrival, neutrophils are primarily responsible for tissue debridement and the clearance of invading microbes, whilst macrophages promote cell recruitment and the removal of apoptotic neutrophils. Given the changes that occur in neutrophil and macrophage function with age, one would predict differences in the inflammatory phase of wound repair between young and older adults. Indeed, in a murine model of dermal injury, Swift et al. reported reduced phagocytic capacity for macrophages isolated from the wounds of aged mice [96], whilst in a cutaneous wound infection model, reduced neutrophil and macrophage numbers in the wounds of aged mice were detected despite no age-related difference in chemokine levels [19]. As neutrophils clear cellular debris, and macrophages, through the clearance of apoptotic neutrophils, reduce bystander tissue damage and initiate the resolution phase of inflammation, innate immunosenescence may be one explanation for the delay in wound healing that accompanies physiological ageing [14].

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