Corticosteroid-binding globulin (CBG): spatiotemporal distribution of cortisol in sepsis

Corticosteroid-binding globulin (CBG) is a 50-60 kDa circulating glycoprotein with high affinity for cortisol. CBG is adapted for sepsis; its cortisol binding is re-duced reversibly by pyrexia and acidaemia, and reduced irreversibly by neutro-phil elastase (NE) cleavage, converting high cortisol-binding affinity CBG to a low affinity form. These characteristics allow for the targeted delivery of immuno-modulatory cortisol to tissues at the time and body site where cortisol is required in sepsis and septic shock. In addition, high titer inflammatory cytokines in sep-sis suppress CBG hepatic synthesis, increasing the serum free cortisol fraction. Recent clinical studies have highlighted the importance of CBG in septic shock, with CBG deficiency independently associated with mortality.

Automated summary

Corticosteroid-binding globulin (CBG) is a circulating glycoprotein that binds to cortisol with high affinity. Its binding capacity is reduced in sepsis by factors such as fever, acidemia, and neutrophil elastase (NE) cleavage. This enables targeted delivery of cortisol to specific tissues during sepsis and septic shock. In addition, inflammatory cytokines in sepsis suppress CBG synthesis, leading to an increase in free cortisol levels. Recent clinical studies have shown that CBG deficiency is associated with increased mortality in septic shock.