68 Chapter 3 inflammatory protein (MIP)-1α), CCL4 (MIP-1β), CCL11 (eotaxin) and GM-CSF were not significantly different from uninjured animals. In burn wound tissue the levels of IL-1β, IL-6, IL-10, TNF-α, CXCL1, CXCL2, CCL2, CCL3 (MIP-1α), epidermal growth factor (EGF), fibroblast growth factor (FGF)2, TGF-β1, VEGF-A and NO were significantly increased. None of the tested inflammatory mediators was decreased in burn wound tissue. The level of IL-1α, histamine and inducible nitric oxide synthase (iNOS) in wound tissue were not significantly different from uninjured animals. Distinct patterns between blood and burn tissue levels were observed: IL-1α and histamine were only increased in blood and CCL3 was only increased in burn tissue. Figure 4. Overall level of inflammatory mediator levels after burn injury. Meta-analysis of the overall levels of cytokines, chemokines, growth factors and other mediators in (A) blood or (B) burn wound tissue at any time after burn injury. Only mediators for which at least 5 studies were available are shown. Results are shown as SMD of levels of inflammatory mediators from burn-injured animals compared to uninjured animals ± CI95%. There is a statistically significant difference with uninjured animals when the CI95% does not cross the x-axis. The I 2 statistic, number of studies and total number of animals used in the burn-injured group for each meta-analysis are shown below the graphs. CI95%, 95% confidence interval; SMD, standardized mean difference. The inflammatory response to burn injury is prolonged in blood and wound tissue To study the effects of burn injury on the levels of inflammatory mediators over time, subgroup analyses were conducted for time intervals after burn (Figure 5). Systemic levels of IL-2 were increased at PBD5-9, while IL-4 was increased directly after injury (PBD
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