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Objectives: This study aimed to evaluate the reactivity and the titers of commercial anti-A and anti-A,B antisera in the detection of A weak antigen expression in human red blood cells., Background: Commercial monoclonal antisera for ABO phenotyping are useful reagents allowing the identification of the four main ABO phenotypes (A, B, AB, and O). However, the reactivity of these commercial reagents can not be evident when the A or B antigens are weakly expressed, and these antisera have low titers., Methods/materials: Six samples from blood donors and five samples from patients with ABO forward and reverse discrepant phenotyping were evaluated. The ABO phenotyping was carried out with different commercial monoclonal anti-A and anti-A,B antisera under different temperatures, using test tubes and gel column agglutination., Results: Monoclonal anti-A antisera with titers less than 256 and anti-A,B with titers less than 128 failed to detect the weak expression of A antigen in 73% and 67% of the A weak phenotypes, respectively. Titres equal to or higher than 2048 (anti-A) and 1024 (anti-A,B) showed better reactivity, independent of the cell clone., Conclusion: Our data indicate that anti-A and anti-A,B antisera with high titers give better reactivity with red blood cells carrying A weak antigen expression., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Background: Malaria clinical outcomes vary by erythrocyte characteristics, including ABO blood group, but the effect of ABO blood group on asymptomatic, uncomplicated and placental Plasmodium falciparum (P. falciparum) infection remains unclear. We explored effects of ABO blood group on asymptomatic, uncomplicated and placental falciparum infection in the published literature., Methods: A systematic review and meta-analysis was performed using the preferred reporting items for systematic reviews and meta-analyses guidelines. Articles in Pubmed, Embase, Web of Science, CINAHL and Cochrane Library published before February 04, 2017 were searched without restriction. Studies were included if they reported P. falciparum infection incidence or prevalence, stratified by ABO blood group., Results: Of 1923 articles obtained from the five databases (Embase = 728, PubMed = 620, Web of Science = 549, CINAHL = 14, Cochrane Library = 12), 42 met criteria for systematic review and 37 for meta-analysis. Most studies (n = 30) were cross-sectional, seven were prospective cohort, and five were case-control studies. Meta-analysis showed similar odds of uncomplicated P. falciparum infection among individuals with blood group A (summary odds ratio [OR] 0.96, 15 studies), B (OR 0.89, 15 studies), AB (OR 0.85, 10 studies) and non-O (OR 0.95, 17 studies) as compared to those with blood group O. Meta-analysis of four cohort studies also showed similar risk of uncomplicated P. falciparum infection among individuals with blood group non-O and those with blood group O (summary relative risk [RR] 1.03). Meta-analysis of six studies showed similar odds of asymptomatic P. falciparum infection among individuals with blood group A (OR 1.05), B (OR 1.03), AB (OR 1.23), and non-O (OR 1.07) when compared to those with blood group O. However, odds of active placental P. falciparum infection was significantly lower in primiparous women with non-O blood groups (OR 0.46, 95% confidence interval [CI] 0.23 - 0.69, I 2 0.0%, three studies), particularly in those with blood group A (OR 0.41, 95% CI 0.003 - 0.82, I 2 1.4%, four studies) than those with blood group O., Conclusions: This study suggests that ABO blood group may not affect susceptibility to asymptomatic and/or uncomplicated P. falciparum infection. However, blood group O primiparous women appear to be more susceptible to active placental P. falciparum infection.

Helicobacter pylori infect millions of people around the world. It occupies a niche in the human gastrointestinal tract characterized by high expression of a repertoire of carbohydrates. ABO and Lewis histo-blood group systems are controlled by genes coding for functional glycosyltransferases which synthesize great diversity of related fucosylated carbohydrate in different tissues, including gastrointestinal mucosa, and exocrine secretions. The structural diversity of histo-blood group carbohydrates is highly complex and depends on epistatic interactions among gene-encoding glycosyltransferases. The histo-blood group glycosyltransferases act in the glycosylation of proteins and lipids in the human gastrointestinal tract allowing the expression of a variety of potential receptors in which H. pylori can adhere. These oligosaccharide molecules are part of the gastrointestinal repertoire of carbohydrates which act as potential receptors for microorganisms, including H. pylori. This Gram-negative bacillus is one of the main causes of the gastrointestinal diseases such as chronic active gastritis, peptic ulcer, and cancer of stomach. Previous reports showed that some H. pylori strains use carbohydrates as receptors to adhere to the gastric and duodenal mucosa. Since some histo-blood group carbohydrates are highly expressed in one but not in others histo-blood group phenotypes it has pointed out that quantitative differences among them influence the susceptibility to diseases caused by H. pylori. Additionally, some experiments using animal model are helping us to understand how this bacillus explore histo-blood group carbohydrates as potential receptors, offering possibility to explore new strategies of management of infection, disease treatment, and prevention. This text highlights the importance of structural diversity of ABO and Lewis histo-blood group carbohydrates as facilitators for H. pylori infection., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Chagas disease, caused by Trypanosoma cruzi, can affect the heart, esophagus and colon. The reasons that some patients develop different clinical forms or remain asymptomatic are unclear. It is believed that tissue immunogenetic markers influence the tropism of T. cruzi for different organs. ABO, Secretor and Lewis histo-blood group systems express a variety of tissue carbohydrate antigens that influence the susceptibility or resistance to diseases. This study aimed to examine the association of ABO, secretor and Lewis histo-blood systems with the clinical forms of Chagas disease. We enrolled 339 consecutive adult patients with chronic Chagas disease regardless of gender (cardiomyopathy: n=154; megaesophagus: n=119; megacolon: n=66). The control group was composed by 488 healthy blood donors. IgG anti-T. cruzi antibodies were detected by ELISA. ABO and Lewis phenotypes were defined by standard hemagglutination tests. Secretor (FUT2) and Lewis (FUT3) genotypes, determined by Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), were used to infer the correct histo-blood group antigens expressed in the gastrointestinal tract. The proportions between groups were compared using the χ2 test with Yates correction and Fisher's exact test and the Odds Ratio (OR) and 95% Confidence Interval (95% CI) were calculated. An alpha error of 5% was considered significant with p-values <0.05 being corrected for multiple comparisons (pc). No statistically significant differences were found for the ABO (X 2 : 2.635; p-value=0.451), Secretor (X 2 : 0.056; p-value=0.812) or Lewis (X 2 : 2.092; p-value=0.351) histo-blood group phenotypes between patients and controls. However, B plus AB Secretor phenotypes were prevalent in pooled data from megaesophagus and megacolon patients (OR: 5.381; 95% CI: 1.230-23.529; p-value=0.011; pc=0.022) in comparison to A plus O Secretor phenotypes. The tissue antigen variability resulting from the combined action of ABO and Secretor histo-blood systems is associated with the digestive forms of Chagas disease., (Copyright © 2016 Elsevier B.V. All rights reserved.)

We investigated the ABO genotypes and heterogeneity of the O alleles in Plasmodium falciparum-infected and non-infected individuals from the Brazilian Amazon region. Sample collection took place from May 2003 to August 2005, from P. falciparum malaria patients from four endemic regions of the Brazilian Amazon. The control group consisted of donors from four blood banks in the same areas. DNA was extracted using the Easy-DNA(TM) extraction kit. ABO genotyping was performed using PCR/RFLP. There was a high frequency of ABO*O01O01. ABO*AO01 was the second most frequent genotype, and the third most frequent genotype was ABO*BO01. There were low frequencies of the ABO*O01O02, ABO*AA, ABO*AB, ABO*BB, and ABO*O02O02 genotypes. We analyzed the alleles of the O phenotype; the O(1variant) allele was the most frequent, both in malaria and non-malaria groups; consequently, the homozygous genotype O(1)(v)O(1)(v) was the most frequently observed. There was no evidence of the homozygous O(2) allele. Significant differences were not detected in the frequency of individuals with the various alleles in the comparison of the malaria patients and the general population (blood donors).

Background and Objective: The basis of blood group A(1) and A(2) phenotypes has been debated for many decades, and still the chemical basis is unresolved. The literature generally identifies the glycolipid chemical differences between blood group A(1) and A(2) phenotypes as being poor or no expression of A type 3 and A type 4 structures on A(2) red cells, although this assertion is not unanimous., Materials and Methods: Using purified glycolipids and specific monoclonal antibodies, we revisited the glycolipid basis of the A(1) and A(2) phenotypes. Purified glycolipids were extracted from four individual A(1) and four individual A(2) blood units. One blood unit from an A weak subgroup was also included. Monoclonal anti-A reagents including those originally used to define the basis of A(1) and A(2) phenotypes were used in a thin layer chromatography - enzyme immunoassay to identify the presence of specific glycolipids., Results: A type 3 glycolipid structures were found to be present in large amounts in all phenotypes. In contrast, the A type 4 glycolipid structure was virtually undetectable in the A(2) phenotype, but was present in the A(1) and A subgroup samples., Conclusion: The major glycolipid difference between the A(1) and A(2) phenotypes is the dominance of A type 4 glycolipids in the A(1) phenotype.

We compared the serological phenotypic frequencies of ABO, MNSs, and Duffy in 417 blood donors and 309 malaria patients from four Brazilian Amazon areas. Our results suggest no correlation between ABO phenotype and malaria infection in all areas studied. We observed significant correlation between the S +s +, S +s -, and S -s + phenotypes and malaria infection in three areas. Some of the Duffy phenotypes showed significant correlation between donors and malaria patients in different areas. These data are an additional contribution to the establishment of differential host susceptibility to malaria.

Context: Epidemiological studies have demonstrated higher frequencies of the O blood group and the non-secretor phenotype of ABH antigens among patients suffering from peptic ulcers. Since Helicobacter pylori has been established as the main etiological factor in this disease, controversies about the associations of the ABO and Lewis blood group phenotypes and secretor and non-secretor phenotypes in relation to susceptibility towards infection by this bacillus have been presented., Objective: To verify the frequencies of ABO, Lewis blood group phenotypes, secretor and non-secretor phenotypes in patients infected or uninfected by H. pylori., Design: Cross-sectional study., Setting: Outpatient clinic., Participants: One hundred and twenty patients with dyspeptic symptoms who underwent endoscopy., Main Measurements: ABO and Lewis blood group phenotypes were determined by a standard hemagglutination test and the secretor and non-secretor phenotypes were evaluated by saliva samples using the inhibitor hemagglutination test., Results: The diagnosis of infection, made via breath and urea tests and confirmed using polymerase chain reaction (PCR) in gastric biopsy fragments, showed the presence of H. pylori in 61.7% of the patients and absence in 38.3%. The differences between the frequencies of the ABO blood group phenotypes among infected (A 27.0%; B 12.2%; AB 4.0% and O 56.8%) and uninfected patients (A 58.7%; B 13.0%; AB 4.3% and O 24.0%) were significant. The Lewis blood type, secretor and non-secretor phenotypes showed homogeneous distribution between the groups of patients analyzed., Conclusions: Our results suggest that the infection of H. pylori can be related to ABO blood groups but not to the Lewis blood group nor to secretor and non-secretor phenotypes.