This article is one of ten reviews selected from the Yearbook of Intensive Care and Emergency Medicine 2010 (Springer Verlag) and co-published as a series in Critical Care. Other articles in the series can be found online at http://ccforum/series/yearbook. Further information about the Yearbook of Intensive Care and Emergency Medicine is available from http://www.springer.com/series/2855.

This article is one of ten reviews selected from the Yearbook of Intensive Care and Emergency Medicine 2010 (Springer Verlag) and co-published as a series in Critical Care. Other articles in the series can be found online at http://ccforum.com/series/yearbook. Further information about the Yearbook of Intensive Care and Emergency Medicine is available from http://www.springer.com/series/2855.

No abstract

No abstract

(77% vs 87%; p<0.03) but this was not a result of complement deficiency as phagocytosis did not depend on whether the bacteria were opsonised or not (73% vs 80%; p¼0.9). The proportion of monocytes capable of generating an oxidative killing burst in response to phagocytosed E coli was markedly reduced (84% vs 47%; p<0.004) in AH patients compared to HC [Abstract PTU-016a figure 1]. Antigen presentation was also impaired: classical monocytes had significantly lower HLA-DR expression in AH compared to controls (73% vs 35%; p¼0.002), with similar levels of HLA-DR expression detected in the CD14+CD16+ monocyte subset (94% vs 74%; p¼0.4).Abstract PTU-016a Figure 1 Conclusion It appears that there are a number of functional defects in circulating monocytes in patients with AH. The marked impairment of phagocytosis and intracellular killing may contribute to the increased susceptibility to infection in this group of patients.