Loss of red cell chemokine scavenging promotes transfusion-related lung inflammation Academic Article uri icon

Overview

MeSH Major

  • Acute Lung Injury
  • Duffy Blood-Group System
  • Erythrocyte Transfusion
  • Erythrocytes
  • Pneumonia
  • Preservation, Biological
  • Receptors, Cell Surface

abstract

  • Red cell transfusions are associated with the development of acute lung injury in the critically ill. Recent evidence suggests that storage induced alterations of the red blood cell (RBC) collectively termed the "storage lesion" may be linked with adverse biologic consequences. Using a 2-event model of systemic endotoxemia followed by a secondary challenge of RBC transfusion, we investigated whether purified RBC concentrates from syngeneic C57BL/6 mice altered inflammatory responses in murine lungs. Transfusion of RBCs stored for 10 days increased neutrophil counts, macrophage inflammatory protein-2 (MIP-2) and chemokine (KC) concentrations in the airspaces, and lung microvascular permeability compared with transfusion of less than 1-day-old RBCs. Because RBCs have been shown to scavenge inflammatory chemokines through the blood group Duffy antigen, we investigated the expression and function of Duffy during storage. In banked human RBCs, both Duffy expression and chemokine scavenging function were reduced with increasing duration of storage. Transfusion of Duffy knockout RBCs into Duffy wild-type endotoxemic mice increased airspace neutrophils, inflammatory cytokine concentrations, and lung microvascular permeability compared with transfusion of Duffy wild-type RBCs. Thus, reduction in erythrocyte chemokine scavenging is one functional consequence of the storage lesion by which RBC transfusion can augment existing lung inflammation.

publication date

  • January 29, 2009

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2635081

Digital Object Identifier (DOI)

  • 10.1182/blood-2008-07-166264

PubMed ID

  • 19064726

Additional Document Info

start page

  • 1158

end page

  • 66

volume

  • 113

number

  • 5