Figure 3.

Enzymatically derived pro-inflammatory AA metabolites are elevated in impaired healing. (A) Lipoxygenase-mediated enzymatic breakdown product cystenyl leukotriene D₄ (cys-LTD₄) was significantly elevated during the first 2 days of healing in LIGHT^−/− mice, suggesting a substantial influx of inflammatory cells. (B) Cystenyl leukotriene E₄ (LTE₄) is involved in increasing inflammation and was found to be elevated when compared to C57BL/6 mice throughout the course of healing. (C) Cyclooxygenase (COX)-mediated breakdown of AA gives rise to exacerbated levels of prostaglandin E2 (PGE₂), which is involved in increased inflammation and neutrophil aggregation, was significantly elevated throughout the course of healing when compared to control C57BL/6 mice. (D) Prostaglandin F2α (PGF_2α) levels had two significantly elevated peaks at days 1 and 3 postwounding. (E) Immunolabeling for COX-2, an enzyme responsible for conversion of AA to prostaglandins. (F) F4/80, a marker for macrophages, to illustrate the presence of inflammation. (G) Merger of (E) and (F) showing that macrophages produced COX-2. (H) COX-2 is shown to be expressed also by keratinocytes. The white line runs along the basement membrane. Propidium iodide staining identifies cell nuclei. (I) COX-2 is also expressed by endothelial cells lining the blood vessels. Scale bar. n = 4. All data are Mean ± SD. *p<0.05, **p<0.01, ***p<0.001. Scale bar 50 μm for (E)–(H) and 10 μm for (I).