Abstract
In this work we have focused on the ability of interleukin-1 to induce an acute phase protein response and a degranulation of polymorphonuclear leukocytes in vivo. The capacity of the interleukin-1 receptor antagonist to influence these events was also investigated. It was shown that interleukin-1 induced an acute phase protein response in rats and mice. In rats α2-macroglubolin levels were increased in plasma after an interleukin-1 injection whereas α1-inhibitor-3 decreased in plasma. In the mice plasma amyloid P was increased. The interleukin-1 receptor antagonist blocked the increase of α2-macroglobulin and plasma amyloid P in a dose dependent way while the effect on the α1-inhibitor-3 decrease was less pronounced. Interleukin-1 led to polymorphonuclear leukocyte degranulation in vivo as measured by increased cathepsin G plasma levels. The interleukin-1 receptor antagonist could influence the early phase of this degranulation.
Highlights
Different forms of tissue injury cause the host to react with a uniform acute phase response
When diisopropylfluorophosphate inactivated cathepsin G was added to normal rat plasma 90% of the added amount could be measured with the assay
In this study we have focused on the ability of IL-1 to induce an acute phase protein response and degranulation of polymorphonuclear leukocyte (PMN) in vivo
Summary
Different forms of tissue injury cause the host to react with a uniform acute phase response This acute phase response is effected by a variety of mediators including different cytokines. Interleukin-1 (IL-1), interleukin-6 (IL-6) and turnout necrosis factor 0 (TNF 0) have been shown to hold central positions in the acute phase response.[2] Several plasma proteins are increased or decreased as a part of the acute phase response. This acute phase protein response differs from species to species. Their main function is to inhibit polymorphonuclear leukocyte (PMN) cathepsin G and elastase, respectively
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