No abstract

Thermal injury causes an increase of circulating IL-1Ra, especially in patients with inhalation injuries. With the current plasma assays for IL-1 beta, IL-1Ra may be a more sensitive marker of human inflammation than IL-1 beta or TNF-alpha.

Abstract. Animal experiments demonstrate that interleukin-lfl (IL-Ib) is beta-cell cytotoxic in vitro and inhibits insulin secretion in vivo. However, it is unknown if IL-ID affects beta-cell function in man. Since IL-Ip and other cytokines are main mediators of the acute phase response, the objectives of the present study were to examine beta-cell function in patients with major burn injuries, and to test if changes in betacell function correlated to systemic levels of IL-IS and tumour necrosis factor ci (TNFol). We established and validated an IL-lB assay measuring free and protein bound IL-Ip; protein bound IL-lP was detached from the IL-Ip specific binding protein by acidification, rendering it accessible for the employed antibody. The IL-1 p specific binding protein (43-60 kDa) was found in serum and plasma from all tested patients and normal subjects. Survivors of burn injuries had a stimulated beta-cell function, whereas non-survivors had an impaired beta-cell function as indicated by an increased plasma concentration of proinsulin, and an increased proinsulin/insulin ratio. In addition, nonsurvivors had significantly increased plasma levels of TL-I/?. However, we could not demonstrate any correlation between C-peptide, proinsulin, insulin or proinsulin/insulin ratio and plasma concentration of IL-1fi.In conclusion, beta-cell function abnormalities are evident in patients with major burn injuries, and a high plasma level of IL-Ip correlates with a fatal outcome. However, the present study did not provide evidence for the hypothesis that beta-cell function is influenced by circulating IL-IB or TNFci during the acute phase response.