The Early Acute Phase Response After Burn Injury in Mice

Abstract

In the hours immediately after burn injury, the body enters into an acute phase reaction characterized, in part, by the augmentation of cytokine and acute phase protein production. This reaction has been poorly characterized in the 24 hours immediately after injury. To better understand the early acute phase response, 8- to 10-week-old BALB/C female mice were subjected to a 15% total body surface area (TBSA). Hepatic levels of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 were monitored. In addition, the circulating level of serum amyloid A, an acute phase protein, also was measured at the same time points. Tumor necrosis factor-alpha levels peaked 2 hours after burn injury, whereas interleukin-1beta had a biphasic response, increasing 2 hours after injury and again at 12 hours. Interleukin-6 and serum amyloid A were not increased until 12 hours after injury and began to decline at 24 hours. These results demonstrate that within the liver, the acute phase response after burn injury initially involves tumor necrosis factor-alpha and interleukin-1beta, whereas interleukin-6 is not involved until later and that systemic serum amyloid A levels are not increased until interleukin-6 is also increased.

Early infection during burn-induced inflammatory response results in increased mortality and p38-mediated neutrophil dysfunction

“…Previous studies in thermally injured mice demonstrate significant systemic increases in TNF-␣ at 6 h postburn and IL-1␤ levels 12 h postburn (11,25). These cytokines are known to prime neutrophils by increasing phosphorylation of p38 (6,40).…”

The role of chicken IL-1β, IL-6 and TNF-α in the occurrence of amyloid arthropathy

“…Proinflammatory cytokines IL-1β, IL-6, and TNF-α, either alone or in combination can increase the production of SAA in mammals (Betts et al 1993;Ray et al 1999;Hagihara et al 2004). IL-1β and IL-6 play an important role in initiating the acute phase response to inflammation in mammals (Hazuda et al 1990;Fujihashi et al 1992;Gauldie et al 1992;Plackett et al 2007). It has also been suggested that IL-6 is as a key cytokine for the induction of AA-amyloidosis in mammals and that IL-6 blocking therapy normalizes the serum SAA levels and appears promising for the treatment of AA-amyloidosis in mammals (Hagihara et al 2004;Mihara et al 2004).…”

Dynamic changes of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 1 after burn injury

“…Severe burns generally associated with systemic inflammatory response syndrome (SIRS) with attributed alteration of proinflammatory and anti-inflammatory cytokines in the early postinsult period [8,9]. Cytokines and growth factors can influence the expression of MMPs and TIMPs significantly [10], and therefore, the balance of MMP-TIMP system could be altered during the early postinjury period.…”