PMID- 8273123
OWN - NLM
STAT- MEDLINE
DCOM- 19940131
LR  - 20190727
IS  - 0041-1132 (Print)
IS  - 0041-1132 (Linking)
VI  - 34
IP  - 1
DP  - 1994 Jan
TI  - Monocyte chemoattractant protein production in red cell incompatibility.
PG  - 16-9
AB  - BACKGROUND: Mononuclear phagocytes play a central role in hemolytic transfusion 
      reactions by erythrophagocytosis and production of inflammatory mediators. 
      Factors that affect the number or function of monocyters would be expected to 
      alter the clinical course of hemolytic transfusion reactions, and thus the 
      production of monocyte chemoattractant protein-1 (MCP-1), a recently described 
      chemotactic and activating cytokine specific for monocytes, was investigated in 
      two distinct settings of red cell (RBC) incompatibility. STUDY DESIGN AND 
      METHODS: Fresh heparinized whole blood was incubated with ABO-compatible or 
      -incompatible RBCs. Isolated peripheral blood mononuclear cells were incubated 
      with anti-D-coated or uncoated RBCs. MCP-1 was measured in the plasma or culture 
      medium by enzyme-linked immunosorbent assay. MCP-1 gene expression was detected 
      by Northern blot analysis of buffy coat or mononuclear cell total RNA. RESULTS: 
      Significant levels of MCP-1 protein in plasma or medium were detected 24 hours 
      after the addition of incompatible RBCs, but not in the first 6 hours. Nonimmune 
      hemolysis of added RBCs did not stimulate MCP-1 production. The inactivation of 
      complement by heat treatment of plasma prior to the addition of RBCs to whole 
      blood did not prevent MCP-1 production. Nor did neutralizing antibodies to tumor 
      necrosis factor prevent MCP-1 production in ABO incompatibility. MCP-1 production 
      was associated with increased steady-state levels of white cell MCP-1 mRNA, which 
      occurred more rapidly in ABO than Rh incompatibility. CONCLUSION: The 
      monocyte-specific chemotactic cytokine MCP-1 is produced by peripheral blood 
      leukocytes in response to RBC incompatibility. MCP-1 may act in a positive 
      feedback loop to recruit and activate monocytes during hemolytic transfusion 
      reactions, thus contributing to the maintenance of these reactions.
FAU - Davenport, R D
AU  - Davenport RD
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor.
FAU - Burdick, M
AU  - Burdick M
FAU - Strieter, R M
AU  - Strieter RM
FAU - Kunkel, S L
AU  - Kunkel SL
LA  - eng
GR  - HL102401/HL/NHLBI NIH HHS/United States
GR  - HL31593/HL/NHLBI NIH HHS/United States
GR  - HL35276/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Transfusion
JT  - Transfusion
JID - 0417360
RN  - 0 (ABO Blood-Group System)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Rh-Hr Blood-Group System)
SB  - IM
GS  - MCP-1
MH  - *ABO Blood-Group System
MH  - Base Sequence
MH  - Blood Group Incompatibility/*metabolism
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*biosynthesis/genetics
MH  - Gene Expression
MH  - Humans
MH  - Molecular Sequence Data
MH  - *Rh-Hr Blood-Group System
MH  - Transfusion Reaction
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - 10.1046/j.1537-2995.1994.34194098596.x [doi]
PST - ppublish
SO  - Transfusion. 1994 Jan;34(1):16-9. doi: 10.1046/j.1537-2995.1994.34194098596.x.