Effect of packed red blood cell transfusion on IL-8 and sICAM-1 in premature neonates at different postnatal ages.

BACKGROUND: Transfusion-related immunomodulation (TRIM) has been described in adults; however, its existence in neonates is not confirmed. The generation of TRIM is attributed to increased concentrations of IL-8, sICAM-1 and other pro-inflammatory cytokines. This study aimed to monitor changes in IL-8, sICAM-1 as markers for TRIM in premature infants at different postnatal ages. METHODS: Preterm infants with a gestational age between 28 and 32 weeks who were receiving PRBC transfusion during the first 28 days of life were included in the study. Infants were stratified into two groups according to their postnatal age: Group 1 with postnatal ages of (0-14) days and Group 2 of (15-28) days. The concentrations of IL-8 and sICAM-1 were measured by enzyme-linked immunosorbent assay (ELISA) before transfusion, 6 h after the end of transfusion and in the donor's PRBCs bag immediately before infusion into the baby. RESULTS: IL-8 concentration in the PRBCs bags correlated with post-transfusion level in Group 2 (r = 0.59, p = 0.002) but not in Group 1 (r = 0.39, p = 0.06). sICAM-1 concentration in the bag correlated with infants'concentrations in neither group. In Group 1, pre-transfusion concentrations of both cytokines (IL-8 and sICAM-1) did not correlate whereas post-transfusion concentrations did correlate (r = -0.09, p = 0.68 and r = 0.4, p = 0.05 respectively). In Group 2, the concentrations of both cytokines did not correlate with each other during pre-transfusion (r = 0.11, p = 0.58) as well as post-transfusion (r = 0.12, p = 0.56). There was no significant increase in either cytokines after transfusion in each group. CONCLUSION: This study showed positive correlation between IL-8 concentration in the transfusion bag and post transfusion in Group 2 infants which could be attributed to passive transmission from the bags. This study does not support an immune modulatory effect for packed RBC in preterm infants.

Association between Duffy antigen receptor expression and disease severity in sickle cell disease patients.

OBJECTIVES: Sickle cell disease (SCD) is associated with a pro-inflammatory state, characterized by an elevated baseline leukocyte count and inflammatory cytokines. Inflammation, white blood cell (WBC) adhesion to vascular endothelium with subsequent endothelial injury, and repeated ischemia-reperfusion injury contribute to disease pathogenesis. Identification of genetic polymorphisms that may modulate disease severity in SCD is becoming a field of interest. The Duffy blood group antigen has been identified as a receptor for various chemokines involved in neutrophil activation and trafficking. This study aimed at investigating the effect of RBCs' Duffy antigen expression and its genetic polymorphisms on modulating disease severity and its complications among Egyptian sickle cell patients. Methods We analyzed the association of Duffy genotypes and phenotypes with clinical expression of SCD in 100 Egyptian patients. The Duffy phenotype expression was detected by indirect anti-globulin test while Duffy genotyping was conducted with polymerase chain reaction-restriction fragment length polymorphism-based assay. Results Total WBC count was strongly associated with Duffy genotype. WBCs were significantly higher in Duffy-positive patients (P = 0.002). No statistical significance was evident between individual measures of disease severity (pulmonary dysfunction, avascular necrosis, central nervous system dysfunction, kidney dysfunction, and leg ulcers) and Duffy genotype. Conclusion Our study suggests that RBC Duffy expression increases levels of WBCs in SCD patients and that Duffy genotype may not be a potential biomarker for end-organ damage in SCD.