Loss of red cell chemokine scavenging promotes transfusion-related lung inflammation

Nilam S. Mangalmurti, Zeyu Xiong, Mei Hulver, Mrunalini Ranganathan, Xiang Hong Liu, Timothy Oriss, Meghan Fitzpatrick, Marc Rubin, Darrell Triulzi, Augustine Choi, Janet S. Leel

Research output: Contribution to journalArticle

97 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1158-1166
Number of pages9
JournalBlood
Volume113
Issue number5
DOIs
StatePublished - Jan 29 2009

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

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