Publications by authors named "Maria do Carmo Valgueiro Costa de Oliveira"

3 Publications

  • Page 1 of 1

Combined genotypes of the MBL2 gene related to low mannose-binding lectin levels are associated with vaso-occlusive events in children with sickle cell anemia.

Genet Mol Biol 2017 Jul-Sep;40(3):600-603. Epub 2017 Aug 21.

Instituto de Ciências Biológicas/Faculdade de Ciências Médicas, Universidade de Pernambuco, Recife, PE, Brazil.

Sickle cell anemia (SCA) presents heterogenous clinical manifestations that cannot be explained solely by alterations to hemoglobin (Hb); other components such as endothelial adhesion, thrombosis and inflammation may be involved. The mannose-binding lectin (MBL) has an important role in innate immunity and inflammatory diseases. In this report, we describe an association between MBL2 polymorphism related to low production of serum MBL and the frequency of vasoocclusive events (FVOE) in children ≤ 5 years old with SCA (p = 0.0229; OR 5.55; CI 1.11-27.66). Further studies are needed to explore the role of low MBL2 in the pathophysiology of vasoocclusive events in SCA.
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August 2017

High Levels of CXCL8 and Low Levels of CXCL9 and CXCL10 in Women with Maternal RhD Alloimmunization.

Front Immunol 2017 3;8:700. Epub 2017 Jul 3.

Hematology and Hemotherapy Foundation of Pernambuco (HEMOPE), Recife, Brazil.

Maternal RhD alloimmunization is an inflammatory response against protein antigens in fetal red blood cells (RBC). However, not all women become alloimmunized when exposed to RhD fetal RBC. Thus, this study aimed to evaluate levels of inflammatory chemokines in RhD pregnant women with erythrocyte alloimmunization. CXCL8, CXCL9, CCL5, and CXCL10 levels were determined from cell culture supernatants by flow cytometry in 46 (30 non-alloimmunized RhD and 16 previously alloimmunized RhD) pregnant women. CXCL8 levels were significantly higher ( < 0.004), and CXCL9 ( < 0.008) and CXCL10 ( < 0.003) levels were significantly lower in alloimmunized pregnant women. No significant difference in CCL5 levels was detected between the groups. Fetal RHD genotyping was performed in the alloimmunized RhD group by real-time PCR. Anti-D alloantibody was detected in 10 mothers and anti-D and -C in six mothers. Twelve fetuses were RHD positive and four were RHD negative. Further studies of serum chemokines and placenta tissue could provide a better understanding of the cells involved in the pathogenesis of maternal erythrocyte alloimmunization.
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July 2017

Molecular Basis of KELnull Phenotype in Brazilians.

Transfus Med Hemother 2015 Jan 19;42(1):52-8. Epub 2014 Dec 19.

Universidade Federal de São Paulo, Hematology and Transfusion Medicine Department, São Paulo, SP, Brazil.

Background: KELnull (K0) persons can produce clinically significant anti-KEL5 antibody after transfusion and/or pregnancy, requiring K0 blood transfusion when indicated. 37 K0 alleles have been reported in studies over different populations, but none in Amerindian-Caucasian descendants from South America. The aim of this study was to identify the molecular basis of K0 phenotype in Brazilians.

Methods: We investigated three K0 samples from different Brazilian blood banks (Recife, Manaus, and Vila Velha) in women with anti-KEL5. KEL antigen typing was performed by serologic techniques, and the K0 status was confirmed by flow cytometry. PCR-RFLP and DNA sequencing of the KEL coding and exon-intron regions were also performed.

Results: RBCs of the 3 patients were phenotyped as KEL:-1,-2,-3,-4,-7. The 3 patients had the same KEL*02/02 genotype and were negative for KEL*02.03 and KEL*02.06 alleles. The Recife K0 patient was homozygous for IVS16 + 1g>a mutation (KEL*02N.31 allele). The flow cytometry with anti-KEL1, anti-KEL2, anti-KEL3, anti-KEL4, and anti-CD238 confirmed the K0 phenotype. In addition, we found the c.10423C>T mutation (KEL*02N.04 allele) in both the Manaus K0 and the Vila Velha K0 patients.

Conclusion: This report represents the first study of K0 molecular basis performed in Amerindian-Caucasian descendants from South America.
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January 2015