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In a previous issue of Critical Care, Giam arellosBourboulis and colleagues published an article in which they drew a conclusion that inhibition of caspase-1 and defective IL-1β production is an important immunological feature in sepsis [1]. Based on the knowledge of previou s research, we would like to make some rema rks. Firstly, peripheral blood mononuclear cells (PBMC) mainly consist of monocytes, T cells, B cells and natural killer cells, of which only monocytes are the high producer of IL-1β and TNFα. Th e proportion of mono cytes in PBMC may therefore greatly aff ect production of these cytokines. In earlier research, Giamarellos-Bourboulis and colleagues demonstrated that the percentage of monocyte apoptosis was over 50% in about half of their septic subjects [2]. In their recent study, however, these authors found that downregulation of IL-1β foll owed a diff erent pattern to TNFα; release of TNFα was not impaired after lipopolysaccharide stimulation of PBMC of patients with uncomplicated sepsis and with severe sepsis [1], suggest ing that the monocytes of these subjects did not undergo apoptosis. Th e introduction of methods to check the apoptosis of monocytes and th eir proportion in PBMC is thus quite necessary. Secondly , the authors concluded that defective IL-1β production is an important immunological feature in sepsis. According to Fahy and colleagues’ research, however, the plasma IL-1β level was signifi cantly elevated in patients with septic shock in comparison with normal control subjects [3]. A possible explanation for this diff erence is that caspase-1 is not the unique enzyme that can activate IL-1β. Recent studies suggest that neutrophils are the major source for processing IL-1β via PR3

Measurement of monocyte apoptosis, plasma IL-1β and PR3 activity as an approach to evaluate the immunological status in sepsis