Chronic Immunosuppression May Increase the Risk of Coronary Artery Perforation in Patients Undergoing CTO-PCI

Background: Anemia is common in premature infants, with RBC transfusion as the treatment for severe cases.Clinical and animal studies suggest a link between anemia, blood transfusion, and brain inflammation.While severe anemia has caused hippocampal injury in animals, the impact of RBC transfusion on brain inflammation post-anemia remains unclear.To identify the inflammatory changes in the neonatal mouse brain of phlebotomy induced anemia and RBC transfusion.Methods: C57BL/6 pups were divided into 4 groups: nave control, RBC transfused, severe anemia, and severe anemia with RBC transfusion.Severe anemia was induced by facial vein phlebotomy on days 2, 4, 6, 8, and 10.RBC transfusion (20 ml/kg) of leukoreduced, stored packed RBC from FVB/NJ donor adult mice was administered intravenously on postnatal day 11 (P11).Brain tissue was collected 24 hours post-transfusion, and protein concentration was measured by bicinchoninic acid (BCA) assay.Cytokines and chemokines were quantified using Milliplex Map Mouse assay.Immunostaining with Ly6c and Iba-1 antibodies was performed to detect monocyte recruitment and microglial activation.Monocyte recruitment in anemic-transfused brains was analyzed by flow cytometry.Results: Inflammatory cytokines IL-1, IL-1, IL-6, TNF-, and IL-12p70 were higher in brain tissues of anemic-transfused mice pups as compared to controls, while IL-4 and IL-5 levels remained unchanged.Chemokines MCP1, MIP1-, MIP1-, RANTES, and Eotoxin were also elevated.Immunostaining revealed increased Ly6C+ monocytes and activated microglia (Iba1+) in the anemic-transfused brain.Flow cytometry confirmed the presence of CD11b+CD45+Ly6C+ monocytes in the anemic-transfused brain. Conclusion:RBC transfusion increases the inflammatory response in murine pups' brains with severe anemia.