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It would be desirable to be able to distinguish fever as a result of febrile non-haemolytic transfusion reactions (FNHTR) from other febrile conditions. To further characterize the inflammatory feature of FNHTR, we measured a large panel of inflammatory markers in pre- and posttransfusion plasma samples from patients with and without FNHTR following the transfusion of leucoreduced red blood cells. As FNHTR patients only displayed a significant increase in IL-6, we conclude that changes in plasma cytokine levels during FNHTR are unlikely to be used diagnostically. An incidental finding of a distinct cytokine pattern in pretransfusion samples from FNHTR patients warrants further investigations, as it might be used to characterize the nature of FNHTR and to predict the risk of these adverse events.

Non-alcoholic steatohepatitis is a highly prevalent liver pathology featured by hepatocellular fat deposition and inflammation. Connexin32, which is the major building block of hepatocellular gap junctions, has a protective role in hepatocarcinogenesis and is downregulated in chronic liver diseases. However, the role of connexin32 in non-alcoholic steatohepatitis remains unclear. Connexin32 −/− mice and their wild-type littermates were fed a choline-deficient high-fat diet. The manifestation of non-alcoholic steatohepatitis was evaluated based on a battery of clinically relevant read-outs, including histopathological examination, diverse indicators of inflammation and liver damage, in-depth lipid analysis, assessment of oxidative stress, insulin and glucose tolerance, liver regeneration and lipid-related biomarkers. Overall, more pronounced liver damage, inflammation and oxidative stress were observed in connexin32 −/− mice compared to wild-type animals. No differences were found in insulin and glucose tolerance measurements and liver regeneration. However, two lipid-related genes, srebf1 and fabp3, were upregulated in Cx32 −/− mice in comparison with wild-type animals. These findings suggest that connexin32-based signalling is not directly involved in steatosis as such, but rather in the sequelae of this process, which underlie progression of non-alcoholic steatohepatitis.