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Leucodepletion and the interaction of polymorphonuclear cells with endothelium in systemic inflammatory response syndrome

Department of Immunobiology, Guy’s, King’s and St Thomas’ Hospital Medical Schools, University College, London

S M Lewis

Department of Immunobiology, Guy’s, King’s and St Thomas’ Hospital Medical Schools, University College, London

T A Hill

Department of Immunobiology, Guy’s, King’s and St Thomas’ Hospital Medical Schools, University College, London

M G Macey

Department of Haematology, The Royal London Hospital, University College, London

D A McCarthey

Department of Haematology, The Royal London Hospital, University College, London

V A Grant

Department of Microbiology, University College, London

D F Treacher

Intensive Treatment Unit, Guy’s and St Thomas’ Hospital NHS Trust, London

The abnormal interaction of polymorphonuclear cells (PMNs) with blood vessel walls is considered to underlie the multiple organ failure of systemic inflammatory response syndrome (SIRS). This consideration is supported by the present finding that PMNs from patients with SIRS are activated, as assessed by an increased distribution of cells bearing CD64, enhanced expression of CD11b and decreased expression of CD62L, and are highly adhesive to endothelial monolayers. Passage of SIRS blood through leucodepletion filters in a laboratory-designed extracorporeal circuit resulted in a marked depletion of PMNs. Of the PMNs that remained in the blood, far fewer cells bound to cultured endothelial cells in comparison with PMNs prior to leucofiltration. We propose that leucofiltration of SIRS blood will limit the number of PMNs available for binding to blood vessel walls and, hence, reduce the pathological manifestations associated with this disorder.

Perfusion, Vol. 16, No. 1 suppl, 75-83 (2001)
DOI: 10.1177/026765910101600i111


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