Elevated monocyte chemoattractant protein‐1 levels following thermal injury precede monocyte recruitment to the wound site and are controlled, in part, by tumor necrosis factor‐α

Abstract

In previous studies, mice given a full-thickness scald injury had an influx of neutrophils into the skin that followed a local increase in a neutrophil chemoattractant. Because macrophages are known to infiltrate the wound area after neutrophils and are essential for normal wound repair, studies were designed to characterize the time course of macrophage accumulation in the wound and to identify the factor(s) responsible for this influx. A macrophage infiltrate into the wound was observed at 4 days post-injury and persisted through at least 10 days. This influx was preceded by an initial fourfold increase in dermal monocyte chemoattractant protein-1 levels at 24 hours post-injury (p < 0.05). This elevation in monocyte chemoattractant protein-1 was enhanced at 4 and 10 days postburn resulting in a sixfold increase over baseline (p < 0.01). Levels of tumor necrosis factor-alpha, a proinflammatory cytokine known to induce chemokine production, were elevated at 90 minutes after injury in burn- versus sham-injured groups (p < 0.05). Furthermore, administration of tumor necrosis factor-alpha neutralizing antibody in vivo reduced the dermal levels of monocyte chemoattractant protein-1 seen at 10 days postburn by 57% (p < 0.01); however, macrophage accumulation was not altered. Thus, elevated systemic TNF-alpha levels may influence the local chemokine milieu following burn injury.

Exercise accelerates cutaneous wound healing and decreases wound inflammation in aged mice

“…Our data add to the growing body of literature that aging inhibits cutaneous wound healing (2,5,8,15,17,18,20,21,30,33,38). More importantly, this study is the first to report that exercise can improve cutaneous wound healing in aged mice and that the improved healing is associated with decreased levels of TNF-␣ and proinflammatory chemokines in the wound tissue.…”

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABAA receptor and dysregulation of p130cas phosphorylation

“…Recruitment of macrophages into wound sites is a critical event for the early stage of wound healing (21,22). Increasing the recruitment of monocytes or macrophages accelerates wound healing (22,60).…”

“…Recruitment of macrophages into wound sites is a critical event for the early stage of wound healing (21,22). Increasing the recruitment of monocytes or macrophages accelerates wound healing (22,60). Inhibition of macrophage phagocytosis with antimacrophage serum also slows wound healing (31), whereas administration of heat shock protein 70, which stimulates macrophage phagocytosis (60), accelerates wound healing (29).…”

“…Although monocytes and macrophages are recruited from peripheral blood to wound sites over time, tissue macrophages are already present within the tissue at the wound site, and phagocytosis of cell debris and contaminated bacteria at the wound site by macrophages is essential for wound repair and prevention of infection (21,22). This process begins early after injury, although it may persist for days thereafter.…”

Stress-induced enhancement of leukocyte trafficking into sites of surgery or immune activation

“…As expected, the magnitude of LTN-induced infiltration of NK cells and T cells was greater than that of neutrophils and macrophages in control NS animals (26). In contrast, the magnitude of TNF-␣-induced infiltration of neutrophils and macrophages was greater than that of NK cells and T cells in control NS animals (27,28). Sponges were retrieved at 6, 24, 48, and 72 h after implantation.…”