Prostaglandin‐Independent Stimulation of Interleukin‐6 Production by Fibrinogen Degradation Product D in Perfused Murine Liver

Abstract

Csala M, Léránt I, Bánhegyi G, Kardon T, Puskás F, Mucha I, Machovich R, Falus A, Mandl J. ProstaglandinIndependent Stimulation of Interleukin-6 Production by Fibrinogen Degradation Product D in Perfused Murine Liver. Scand J Immunol 1998;48:269-271 Bacterial endotoxin (LPS) and fibrinogen degradation product D (FDP-D) are both potent stimulators of interleukin-6 (IL-6) production in liver, however, there are differences in their metabolic effects. The aim of the present study was to compare the role of prostaglandins in the enhancement of IL-6 production by LPS or FDP-D in perfused mouse livers. Indomethacin inhibited the effect of LPS significantly but was ineffective in the case of FDP-D. Accordingly, production of prostaglandins D 2 and E 2 was not elevated following the addition of FDP-D, while their formation was increased several fold by LPS. At the same time interleukin-1 (IL-1) production in perfused liver rose markedly upon the addition of FDP-D. It is suggested that prostaglandins are not involved in the effects of FDP-D on the liver. The stimulatory effect of FDP-P on IL-6 production might be the consequence of elevated IL-1 levels.

Plasma D-Dimer Levels Are Associated with Stroke Subtypes and Infarction Volume in Patients with Acute Ischemic Stroke

“…Secondly, some markers of hemostatic function are acute-phase reactants; D-dimer is one of these markers. There is, in fact, some evidence that fibrin degradation products, including D-dimer, may act to stimulate the inflammatory process [39], and this might provide a further pathological mechanism through which D-dimer is linked to progressing stroke [40]. There is some evidence that D-dimer itself stimulates monocyte synthesis and release of proinflammatory cytokines such as interleukin- 6[41].…”

Plasma D-Dimer Predicts Short-Term Poor Outcome after Acute Ischemic Stroke

“…Second, D-D may stimulate the inflammatory process. Activated inflammation and activated coagulation, in concert with each other, may contribute to the development of unfavorable outcome [30]. Furthermore, high D-D levels may be resistant to the endogenous fibrinolytic system [31].…”

Hemostatic Function and Progressing Ischemic Stroke

“…Adjustment of the association of D-dimer with progressing stroke for these inflammatory indices did not account for the association. There is, in fact, some evidence that fibrin degradation products, including D-dimer, may act to stimulate the inflammatory process, [25][26][27][28] and this might provide a further pathological mechanism through which D-dimer is linked to progressing stroke. 29,30 The finding that admission mean arterial blood pressure independently predicts progressing stroke is interesting.…”