Evaluation of Sequential Serum Interleukin-6 Levels in Liver Allograft Recipients

Abstract

Control serum levels of IL-6 measured by ELISA in 30 healthy blood donors or volunteers were 18±S4 pg/ml (mean ± SD). Pretransplant serum levels of IL-6 in 169 adult candidates for liver transplantation were significantly higher than control in those with fulminant hepatitis (203±232 pg/ml), alcoholic cirrhosis (116±257 pg/ml), and hepatocellular carcinoma (82±105 pg/ml). With these data as background, plasma or serum levels of EL-6 were monitored in 24 adult patients after first OLT and correlated with the clinical courses and the histopathological diagnosis of rejection. Serum or plasma levels of IL-6 decreased after transplantation regardless of pretransplant value. Four patients with infection subsequently developed continuously high IL-6 values. In the 20 of 24 patients who did not have infection, significantly higher levels of IL-6 were consistently found 0-4 days before histopathological diagnosis of rejection (131±78 pg/ml) compared with significantly lower values in patients without rejection episodes (40±21 pg/ml). The elevations of IL-6 were spike shaped, did not correlate well with the histopathological grades of rejection, and were highly responsive to augmented immunosuppression. These 20 cases were classified as: group 1, no spikes of IL-6 after liver transplantation; group 2, single spike of IL-6 after liver transplantation; and group 3, multiple spikes of IL-6 after liver transplantation. The combined early and late graft loss of each group was 0% (group 1), 25% (group 2), and 67% (group 3). We conclude that daily monitored serum or plasma IL-6 levels can be a good premonitor of liver allograft rejection and also a useful predictor of long-term graft outcome.

Inflammatory markers sampled by microdialysis catheters distinguish rejection from ischemia in liver grafts

“…Interestingly, these 2 inflammatory mediators, which counteract each other, closely reflect ischemia/reperfusion, and this indicates that the inflammatory network functions to balance the detrimental effects of this condition. CXCL8, a chemokine,47 and IL‐6, a proinflammatory cytokine,48 increased with ischemia, but a positive trend was also detected with rejection. This indicates that these mediators are expressed by a general activation of the immune system and not specifically by the adaptive (cell‐mediated) or innate immune system.…”

Th17 promotes acute rejection following liver transplantation in rats

“…It is well known that IL-6 plays an important role in the regulation of inflammatory and immunological responses (Kishimoto, 1989). Kita et al (1994) and Warlé et al (2003) reported that IL-6 expression was markedly elevated during liver allograft rejection. The present study displayed a close correlation between IL-6 and IL-17.…”

Biomarkers for the diagnosis of acute cellular rejection in liver transplant recipients: A review

“…Kita et al . observed in contrast a marked rise of IL‐6 during ACR and during infection, however, the rise pattern was distinguishable between both …”

“…Kita et al observed in contrast a marked rise of IL-6 during ACR and during infection, however, the rise pattern was distinguishable between both. 23 Interleukin-15 is produced by non-lymphatic cells including macrophages, dendritic cells and epithelial cells. Its biologic activities are similar to those of IL-2.…”