SIR ROBERT MUIR, SEPSIS AND SCOTTISH HEALTHCARE

If a patient survives the initial huge immune onslaught against the invading micro-organism in the blood-stream, immunosuppression can then occur. The exact timing of immunosuppression is a controversial topic still under debate. Some scientists consider that immune suppression must be initiated after hyper-inflammation, whereas others believe that immunosuppression is a consequence of hyper-inflammation. Multiple papers have shown that some sepsis patients very quickly generate both pro-inflammatory and anti-inflammatory cytokines, and other patients either produce a huge amount of anti-inflammatory cytokines or present with universally reduced cytokine manufacture. Hotchkiss et.al harvested tissues from patients dying of sepsis and found huge apoptosis induced loss of immune cells, such as CD4 and CD8 T cells, B cells and dendritic cells. At this stage of infection, it would be hoped that the body was fighting infection, rather than depleting the immune response. Substantial loss of effector immune cells is a global finding in all age groups during sepsis. Anti-apoptotic therapies have been shown to be effective preventers of immune effector cell death and have also been shown to prevent death in animal models of sepsis. Anti-apoptotic drugs may become septicaemia therapies in future.