FUT2 Research Articles

OP39 The effect of phenotype and genotype on the plasma proteome in patients with Inflammatory Bowel Disease

Abstract Background Protein profiling in patients with inflammatory bowel diseases (IBD) for diagnostic and therapeutic purposes is underexplored. Assessment of interactions between genetics and the plasma proteome could lead to identification of novel disease-associated molecular pathways. In this study, we performed the largest gene-protein association analysis thus far in patients with IBD, taking into account relevant phenotypic covariates and integrating information from multiple biological data layers. Methods Ninety-two (92) inflammation-related proteins were quantified in plasma of 1,028 patients with IBD (567 Crohn’s disease [CD]; 461 ulcerative colitis [UC]) and 148 healthy individuals to assess proteome-phenotype associations. Both whole-exome sequencing (WES) and global screening array (GSA) data of 919 patients with IBD were included to study associations between over 8 million genetic variants and protein levels (protein quantitative trait loci [pQTL]). Cis-pQTLs were defined within ± 1 Mb of the region of each protein-coding gene center, whereas trans-pQTLs were outside of that region. After adjusting for phenotypic covariates, a step-wise conditional analysis was used to identify all independent pQTLs in CD and UC separately, followed by a meta-analysis. Intestinal mucosal RNA sequencing and fecal metagenomic data were used for complementary analyses. Results Thirty-four (34) proteins were differentially abundant between IBD and healthy individuals, of which 24 proteins independent of active inflammation. (Figure 1) Seventy-two (72) proteins were significantly associated to 14 phenotypic factors, including age, sex, medication use, and surgical history. (Figure 2) Fibroblast growth factor-19 (FGF-19) levels were decreased in CD patients with ileal disease or a history of ileocecal resection. Thirteen (13) novel cis-pQTL variants were identified and 10 replicated from previous studies, together affecting 21 different plasma proteins. One trans-pQTL variant of the FUT2 gene (rs602662) and two independent cis-pQTL variants of the CCL25 gene significantly affected plasma C-C motif chemokine ligand 25 (CCL25) levels. (Figure 3) Intestinal gene expression data revealed an overlapping cis-expression (e)QTL-variant (rs3745387) of the CCL25 gene. The FUT2 rs602662 trans-pQTL variant associated significantly with reduced abundances of multiple fecal butyrate-producing bacteria, including the genus Blautia and the species Faecalibacterium prausnitzii. Conclusion This study shows that both genotype and multiple disease phenotypes strongly associate with the plasma proteome in patients with IBD and identifies disease-associated pathways that may help to improve disease management in the future.

Serological and molecular biological analysis of an individual with para-Bombay blood group due to homozygous c.948C>A variant of FUT1 gene

To study the serological, molecular and genetic characteristics of an individual with para-Bombay blood group. Serological method was used to detect the presence of A, B, H antigens in red blood cells and saliva, and Sanger sequencing was used to analyze the FUT1 gene of the proband and her family members. Genetic mechanism of the blood group was analyzed by pedigree analysis. Forward and reverse typing of the ABO blood group were inconsistent for the proband. A, B and H antigens were not found on erythrocytes, while B and H antigens were found in saliva, in addition with unexpected antibodies. The proband was found to have a genotype of ABO*B.01/ABO*O.01.04 caused by homozygous variant of c.948C>A (p.Tyr316Ter) of the FUT1 gene. A novel para-Bombay blood group was identified, which was due to the missense variant of c.948C>A in the coding region of the FUT1 gene, which has probably resulted in inability to synthesis active H antigen transferase.

Altered gut microbiome in FUT2 loss‐of‐function mutants in support of personalized medicine for inflammatory bowel diseases

Background & Aims FUT2 encodes an α-1,2-fucosyltransferase required for the proper production of oligosaccharides and glycoproteins. The FUT2 polymorphism has been hypothesized to mediate a genetic mechanism to impact gut microbiota and consequently contribute to IBD pathogenesis, because of the high prevalence of loss-of-function polymorphisms of FUT2 and their association with IBD in genome-wide association studies. In this study, we investigated the role of the gut microbiota in IBD patients with FUT2 loss-of-function mutation. Method A total of 81 inflammatory bowel disease (IBD) patients were enrolled in 6th Affiliated Hospital of Sun Yat-sen University in Guangzhou, China between March 2016 and July 2018. To determine the genotypes of the patients at rs1047781 (A385T) and rs601338 (G428A) of the FUT2 gene, individuals were asked to provided blood samples. All participants were divided into 3 groups according to their genotypes: SeSe, Sese, and sese groups. For microbiome study, fecal DNA was collected and the V5-V6 region of the 16S rDNA was sequenced with a MiSeq platform. Metabolomics analysis targeting SCFA was performed by gas chromatography. Result The FUT2 genotypes are associated with specific gut microbiome compositions and functions in IBD patients. Differences in alpha-, beta-diversities, bacterial abundances at every taxonomic levels were observed between different FUT2 genotypes. Escherichia was significantly decreased in the gut of the sese patients. On the other hand, CD8+ inducing Alistipe and Phascolarctobacterium and Th17 inducing Erysipelotrichaceae were more abundant in sese patients suggests that these bacteria may explain the higher incidence of IBD among sese individuals. The PICRUSt functional analysis based on the 16S data showed that, several carbohydrate synthesis pathways were enriched in IBD patients with non-functional mutation of FUT2 (P<0.05). Interestingly, SCFA-producing bacteria in sese patient were not decreased although SCFA is protective against colon inflammation. Metabolomics analysis targeting SCFA confirmed this observation. Discussion Data presented here explained the association of non-secretor status with IBD. Our study supports the hypothesis that FUT2 loss-of-function genotype causes altered gut microbiota that is poised to the development of IBD. The identification of the T cell inducing species in this study contributes to the knowledge base for the development of personalized microbial intervention for IBD.

Gut microbiota-mediated lysophosphatidylcholine generation promotes colitis in intestinal epithelium-specific Fut2 deficiency

Background and aimsPrevious study disclosed Fucosyltransferase 2 (Fut2) gene as a IBD risk locus. This study aimed to explore the mechanism of Fut2 in IBD susceptibility and to propose a new strategy for the treatment of IBD.MethodsIntestinal epithelium-specific Fut2 knockout (Fut2△IEC) mice was used. Colitis was induced by dextran sulfate sodium (DSS). The composition and diversity of gut microbiota were assessed via 16S rRNA analysis and the metabolomic findings was obtained from mice feces via metabolite profiling. The fecal microbiota transplantation (FMT) experiment was performed to confirm the association of gut microbiota and LPC. WT mice were treated with Lysophosphatidylcholine (LPC) to verify its impact on colitis.ResultsThe expression of Fut2 and α-1,2-fucosylation in colonic tissues were decreased in patients with UC (UC vs. control, P = 0.036) and CD (CD vs. control, P = 0.031). When treated with DSS, in comparison to WT mice, more severe intestinal inflammation and destructive barrier functions in Fut2△IEC mice was noted. Lower gut microbiota diversity was observed in Fut2△IEC mice compared with WT mice (p < 0.001). When exposed to DSS, gut bacterial diversity and composition altered obviously in Fut2△IEC mice and the fecal concentration of LPC was increased. FMT experiment revealed that mice received the fecal microbiota from Fut2△IEC mice exhibited more severe colitis and higher fecal LPC concentration. Correlation analysis showed that the concentration of LPC was positively correlated with four bacteria—Escherichia, Bilophila, Enterorhabdus and Gordonibacter. Furthermore, LPC was proved to promote the release of pro-inflammatory cytokines and damage epithelial barrier in vitro and in vivo.ConclusionFut2 and α-1,2-fucosylation in colon were decreased not only in CD but also in UC patients. Gut microbiota in Fut2△IEC mice is altered structurally and functionally, promoting generation of LPC which was proved to promote inflammation and damage epithelial barrier.

Survey and characterization of nonfunctional alleles of FUT2 in a database

The expression of ABO antigens in human saliva is regulated by the FUT2 gene, which encodes a secretor type α(1,2)fucosyltransferase. Secretors express ABO substrates in saliva and non-secretors do not. Secretor status is an object of concern, especially for susceptibility to various infectious diseases. A multitude of single nucleotide polymorphisms (SNPs) and copy number variations (CNVs) have been reported, and they show unique distributions among different populations. In this study, we selected 18 uncharacterized FUT2 alleles listed in the Erythrogene database and obtained genomic DNA having these alleles. We experimentally confirmed the haplotypes, but 10 of 18 alleles disagreed with those in the database, which may be attributed to their low frequency. We then examined the activity of the encoded α(1,2)fucosyltransferase for 13 alleles by flow cytometry of H antigen expression. The impact of each nonsynonymous SNP on the enzyme was also estimated by software. We finally identified two non-secretor alleles (se610and se357,856,863) and one weak secretor allele (se262,357), while in silico analysis predicted that many alleles impair the function. The present results suggest that correct haplotyping and functional assays are desirable for analysis of the FUT2 gene.

Enteric Viruses and Inflammatory Bowel Disease.

Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is a multifactorial disease in which dietary, genetic, immunological, and microbial factors are at play. The role of enteric viruses in IBD remains only partially explored. To date, epidemiological studies have not fully described the role of enteric viruses in inflammatory flare-ups, especially that of human noroviruses and rotaviruses, which are the main causative agents of viral gastroenteritis. Genome-wide association studies have demonstrated the association between IBD, polymorphisms of the FUT2 and FUT3 genes (which drive the synthesis of histo-blood group antigens), and ligands for norovirus and rotavirus in the intestine. The role of autophagy in defensin-deficient Paneth cells and the perturbations of cytokine secretion in T-helper 1 and T-helper 17 inflammatory pathways following enteric virus infections have been demonstrated as well. Enteric virus interactions with commensal bacteria could play a significant role in the modulation of enteric virus infections in IBD. Based on the currently incomplete knowledge of the complex phenomena underlying IBD pathogenesis, future studies using multi-sampling and data integration combined with new techniques such as human intestinal enteroids could help to decipher the role of enteric viruses in IBD.

Estrus Behaviour and Reproductive Traits of Pulawska Gilts Associated with Selected Gene Polymorphisms

Abstract Searching for the associations between the gene polymorphism and the reproductive traits is essential in defining the genetic native breed specificity, which distinguishes them from the other breeds. The aim of our study was to determine the associations between mutations in the PRL, PRLR, PTGS2, FUT1 genes and sexual and periparturient activity in native Pulawska gilts. The analysis included 72 animals which gave birth to the first litter. Evaluation of the productive value of gilts accounted for indicators of sexual and periparturient activity as well as reproductive traits. The biological material for molecular analyses was obtained from the hair roots of the gilts. The genotype was verified by PCR RFLP analysis. The primers and PCR conditions were determined on the basis of available literature data. Statistically significant differences (P≤0.05) were found at the PRL locus: gilts of AA genotypes (Ins/Ins) at the PRL locus were characterised by longest farrowing duration compared to gilts of AB genotype (P≤0.05). The analysis of PRLR gene showed that gilts of TT genotype revealed a tendency for later occurrence of estrus signs (first and second estrus) and for the markedly longest farrowings (P≤0.05). With regard to PTGS2 and FUT1 loci, no significant differences were found in the parameters of sexual and periparturient activity of the gilts. However, gilts of FUT1 GG genotype gave birth to and reared the largest first litters (P≤0.05). The results of the studies expand the knowledge about the genetic structure and productivity of Pulawska gilts.

Genetic Studies of Natural Glycosphingolipid Ligands for NKT Cells.

Glycosphingolipids (GSL) are natural ligands of NKT cells. Several laboratories have reported the in vitro activity of isoglobotriosylceramide (iGb3) in stimulating NKT cells. However, the knockout mice of iGb3 synthase showed no deficiency in development and function of NKT cells. There is a lack of knowledge on the genetics of redundant natural glycosphingolipid ligands. We have identified additional glycosphingolipid with stimulatory activity to NKT cells, including fucosyl lactosylceramide (H antigen). Here we describe the procedures to generate mice with deficiencies in Fut1, Fut2, and Sec1 genes to deplete H antigen through BAC engineering for the generation of ES cell-targeting construct, as well as the mice with deficiency of both blood group H-GSL ligand and isoglobotriosylceramide.

Can the FUT2 Non-secretor Phenotype Associated With Gut Microbiota Increase the Children Susceptibility for Type 1 Diabetes? A Mini Review.

The global toll of type 1 diabetes (T1D) has steadily increased over the last decades. It is now widely acknowledged that T1D pathophysiology is more complex than expected. Indeed, a multifaceted interplay between genetic, metabolic, inflammatory and environmental factors exists that leads to heterogeneous clinical manifestations across individuals. Children with non-secretor phenotype and those affected by T1D share low abundance of bifidobacteria, low content of short-chain fatty acids, intestinal phosphatase alkaline and a high incidence of inflammatory bowel diseases. In this context, host-gut microbiota dyad may represent a relevant contributor to T1D development and progression due to its crucial role in shaping host immunity and susceptibility to autoimmune conditions. The FUT2 gene is responsible for the composition and functional properties of glycans in mucosal tissues and bodily secretions, including human milk. FUT2 polymorphisms may profoundly influence gut microbiota composition and host susceptibility to viral infections and chronic inflammatory disease. In this minireview, the possible interplay between mothers' phenotype, host FUT2 genetic background and gut microbiota composition will be discussed in perspective of the T1D onset. The study of FUT2-gut microbiota interaction may add a new piece on the puzzling T1D etiology and unveil novel targets of intervention to contrast T1D development and progression. Dietary interventions, including the intake of α-(1, 2)-fucosyl oligosaccharides in formula milk and the use of specific prebiotics and probiotics, could be hypothesized.

Investigating the causal effect of maternal vitamin B12 and folate levels on offspring birthweight.

BackgroundLower maternal serum vitamin B12 (B12) and folate levels have been associated with lower offspring birthweight, in observational studies. The aim of this study was to investigate whether this relationship is causal.MethodsWe performed two-sample Mendelian randomization (MR) using summary data on associations between genotype-B12 (10 genetic variants) or genotype-folate (four genetic variants) levels from: a genome-wide association study of 45 576 individuals (sample 1); and both maternal- and fetal-specific genetic effects on offspring birthweight from the latest Early Growth Genetics consortium meta-analysis with 297 356 individuals reporting their own birthweight and 210 248 women reporting their offspring's birthweight (sample 2). We used the inverse variance weighted method, and sensitivity analyses to account for pleiotropy, in addition to excluding a potentially pleiotropic variant in the FUT2 gene for B12 levels.ResultsWe did not find evidence for a causal effect of maternal or fetal B12 levels on offspring birthweight. The results were consistent across the different methods. We found a positive causal effect of maternal folate levels on offspring birthweight [0.146 (0.065, 0.227), which corresponds to an increase in birthweight of 71 g per 1 standard deviation higher folate]. We found some evidence for a small inverse effect of fetal folate levels on their own birthweight [−0.051 (−0.100, −0.003)].ConclusionsOur results are consistent with evidence from randomized controlled trials that higher maternal folate levels increase offspring birthweight. We did not find evidence for a causal effect of B12 levels on offspring birthweight, suggesting previous observational studies may have been confounded.

Estimation of genetic variation in the Secretor and Lewis genes in Iranian hospitalized children.

The Secretor (FUT2) and lewis gene (FUT3) are in charge of the construction of histo-blood group antigens, which act as a receptor for some Pathogenes. This study aimed to estimate the prevalence of five significant single nucleotide polymorphisms (SNPs) in Iranian children. In this cross-sectional study, 102 blood samples collected from hospitalized children. The FUT2 gene region was amplified and sequenced to explore rs1047781 and rs601338, and the FUT3 gene region was amplified to explore rs28362459, rs812936, rs778986 SNPs. In FUT2 gene, Se358,428 that produces Se phenotype with 63% (0.53 - 0.72) prevalence, was the most common genotype. For FUT3 gene Le59,202,314 with 80% prevalence was most common genotype (0.71 - 0.87). This study genotyped Secretor and Lewis genes and designated SNPs' distinct distribution in Iran, and clarified at-risk groups for certain diseases.

Blood group systems

Blood group systems

Two novel FUT1 alleles that cause para-Bombay phenotype in a Chinese individual.

Bombay and para-Bombay phenotypes, which arise from gene mutations of α-1,2-fucosyltransferase FUT1, are very rare in Chinese population. A para-Bombay phenotype Chinese individual with two novel FUT1 mutations was reported here. The peripheral blood and saliva samples of the proband and her family members were collected after informed consent. ABO and H blood group phenotyping was performed by haemagglutination methods. ABO genotype was determined by PCR-SSP kit. A, B, and H antigens in saliva were detected by a hemagglutination inhibition test. Fragments encompassing the full coding region of FUT1 and FUT2 genes were PCR amplified and sequenced. Allelic sequences were validated by cloning and sequencing individual colonies. The serologic reaction results of the proband revealed that A, B, and H antigen were absent on RBCs, but B and H antigen were presented in saliva, and the serum contains anti-H. The proband was assigned as B/O1 by ABO genotyping. Two new heterozygous mutations of FUT1 gene, c.508dupT and c.787A>C, were identified through direct sequencing of PCR-amplified products. TA cloning and sequencing confirmed that two novel mutations were on different alleles. FUT2 gene sequence of the proband is consistent with standard. The other family members of the proband showed normal phenotypes of ABO blood group and their genotypes are consistent with phenotypes. Two novel FUT1 alleles, with the previously not reported mutations c.508dupT and c.787C, respectively, are responsible for the para-Bombay phenotype detected in the sample from the proband.

Dynamic Transcriptome Reveals the Mechanism of Liver Injury Caused by DHAV-3 Infection in Pekin Duck.

Duck hepatitis A virus 3 (DHAV-3) is a wild endemic virus, which seriously endangers the duck industry in China. The present study aims to elucidate the mechanism of duck resistance to DHAV-3 infection. Both resistant and susceptible ducks were challenged with DHAV-3 in this experiment. The histopathological features and serum biochemical indices (ALT and AST) were analyzed to estimate liver injury status at 6, 12, 15, and 24 h post-infection (hpi). The dynamic transcriptomes of liver were analyzed to explain the molecular regulation mechanism in ducks against DHAV-3. The result showed that the liver injury in susceptible ducks was more serious than that in the resistant ducks throughout the four time points. A total of 2,127 differentially expressed genes (DEGs) were identified by comparing the transcriptome of the two populations. The expression levels of genes involved in innate immune response increased rapidly in susceptible ducks from 12 hpi. Similarly, the expression of genes involved in cytokine regulation also increased at the same time points, while the expression levels of these genes in resistant ducks remained similar between the various time points. KEGG enrichment analysis of the DEGs revealed that the genes involved in cytokine regulation and apoptosis were highly expressed in susceptible ducks than that in resistant ducks, suggesting that excessive cytokine storm and apoptosis may partially explain the mechanism of liver injury caused by DHAV-3 infection. Besides, we found that the FUT9 gene may contribute to resistance towards DHAV-3 in resistant ducklings. These findings will provide insight into duck resistance and susceptibility to DHAV-3 infection in the early phases, facilitate the development of a strategy for DHAV-3 prevention and treatment, and enhance genetic resistance via genetic selection in animal breeding.

Can the FUT 2 Gene Variant Have an Effect on the Body Weight of Patients Undergoing Bariatric Surgery?—Preliminary, Exploratory Study

Background: The FUT2 gene (Se gene) encoding the enzyme α-1,2-L-fucosyltransferase 2 seems to have a significant effect on the number and type of bacteria colonizing the intestines. Methods: In a group of 19 patients after bariatric surgery, the polymorphism (rs601338) of FUT2 gene was analyzed in combination with body mass reduction, intestinal microbiome (16S RNA sequencing), and short chain fatty acids (SCFA) measurements in stools. Results: Among the secretors (Se/Se polymorphism of the FUT2 gene rs601338, carriers of GG variant), correlations between waist-hip ratio (WHR) and propionate content and an increase in Prevotella, Escherichia, Shigella, and Bacteroides were observed. On the other hand—in non-secretors (carriers of GA and AA variants)—higher abundance of Enterobacteriaceae, Ruminococcaceae, Enterobacteriaceae, Clostridiales was recorded. Conclusions: The increased concentrations of propionate observed among the GG variants of FUT 2 may be used as an additional source of energy for the patient and may have a higher risk of increasing the WHR than carriers of the other variants (GA and AA).

Associations between fucosyltransferase 3 gene polymorphisms and ankylosing spondylitis: A case–control study of an east Chinese population

Many susceptibility genes of inflammatory bowel disease (IBD) are associated with ankylosing spondylitis (AS). Fucosyltransferase 2 (FUT2) and FUT3 genes are related to IBD. This study aimed to investigate whether these genes correlated with the susceptibility to AS. Questionnaires of 673 patients with AS, and peripheral blood specimens of the patients and 687 healthy controls were collected. FUT2 and FUT3 genes were genotyped using the SNPscan method. Frequency differences of the genes at different levels, haplotypes, and interactions were analyzed. No frequency differences were found between the cases and the controls in all the genotypes and the alleles of rs1047781, rs1800028, rs1800030, and rs812936. For rs28362459, a significant difference in allele frequencies was observed in the total participants between the groups [χ2 = 7.515, Pcorrected = 0.030; adjusted odds ratio (ORadjusted)G/T = 0.782; 95% confidence interval (CI), 0.650–0.941]. The frequencies of haplotypes TT (rs812936–rs28362459) (χ2 = 5.663, Ppermutation = 0.039) and TG (rs812936–rs28362459) (χ2 = 7.456, Ppermutation = 0.013) in the total participants, and TG (rs812936–rs28362459) in the female subgroup (χ2 = 5.624, Ppermutation = 0.047) showed significant differences between the cases and the controls. No frequency differences at the phenotypic level were found. Two-factor interactions were observed between rs28362459-TG and age, rs28362459-TG and sex, rs28362459 and rs1047781, and the Lewis and secretor status. Rs28362459-G was related to some aggravated symptoms of AS (all Pcorrected < 0.05). These findings indicated that FUT3 polymorphisms were associated with human predisposition to AS at the allele and haplotype level. Rs28362459-G might decrease the susceptibility to AS, but aggravate relevant symptoms.

Key genes involved in utilization of highly abundant HMO in breastmilk are present in B. infantis EVC001 allowing for superior colonization of the breastfed infant gut compared to other commercial probiotic strains

Purpose: Breast milk contains a high concentration of complex glycans known as human milk oligosaccharides (HMO). HMO influence the composition of the intestinal microbiome of breastfed infants by serving as growth substrates to select strains of bifidobacteria. More than 200 individual HMO structures have been identified in breastmilk. However, lacto-N-tetraose (LNT), lacto-N-neotetraose (LNnT), and 2’-Fucosyllactose (2’FL) in FUT2+ mothers, are disproportionally abundant. The biological role for their abundance in the context of bacterial colonization of the infant gut has not been determined. In a previous study, Bifidobacterium …

Polymorphism of Congjiang Pigs FUT1 Gene and Its Association with Carcass and Meat Quality Traits

In order to investigate the effects of the M229 and M307 locus in FUT1 gene on the carcass and meat quality of Congjiang pigs. In this study, PCR-SSCP, PCR-RFLP and direct sequencing methods were used to quickly type the M229 and M307 loci, and then the association between different genotypes and meat traits was analysed. Population genetic structure analysis showed that M229 locus of FUT1 gene was in Hardy-Weinberg equilibrium, with high polymorphism information content, rich genetic diversity and large space for directional breeding. However, the M307 locus had the opposite result, showing a skewed distribution. Correlation analysis showed that the average backfat thickness index of CT and TT genotypes from the M229 locus of FUT1 gene in Congjiang pigs was significantly lower than that of CC (P <0.05). The conclusion of this experiment indicates that the M229 locus of FUT1 gene can be strengthened in Congjiang pigs, which can be used for breeding applications.

THE PRESENCE OF A POTENTIAL PATIENT OF COLIBACTERISIS IN THE POPULATION OF PIGS OF LOCAL SELECTION OF UKRAINIAN MEAT BREED

Each year about 10 million piglets die all over the world because of oodema disease and postweaning diarrhea. These diseases associated with the adhesion of enterotoxic Escherichia coli on the surface of pig intestinal cells are called colibacteriosis. The disease exciter is enteropathogenic hemolytic strains of Eschenchia (E. coli). The enterotoxic E. coli O157 is able to produce specific adhesins in piglet colibacteriosis, the most important role being played by F18 and F4 (K 88). The genetic resistance of piglets to diarrhea is based on the lack of appropriative receptors on the surface of the intestinal cells of animals. It is practical interest in pigs breading to study using polymorphism of E. coli F18 and F4 (ECR F18/FUT1 and ECR F4/MUC4) receptor genes in the selection process associated with the occurrence of colibacteriosis in piglets. The studies were apropiate on the basis of a breeder reproducer of the Ukrainian meat breed pigs of Dnipropetrovsk state agricultural institute selection at "Lugovskoye" Ltd. of firm "Avias 2000" of Solonyansky district, Dnipropetrovsk region. Microbiological studies of the presence of E. coli O157 in the animals faeces were performed at the Department of Biotechnology of the Ukrainian Chemical Technology University, using a ready-made selective Compact Dry EC medium. Animal genotype estimation for FUT1 and MUC4 genes was carried out at the genetic laboratory of the Institute of Pig Breeding andAgro Industrial Production, National Academy of Agrarian Sciences of Ukraine, by the PCR-RFLP method. Studies have been conducted to detect enterotoxigenic E. coli O157 in a closed population of pigs of Ukrainian meat breed type of selection of Dnepropetrovsk state agricultural institute. 58.3% of clinically healthy sows were found to contain E. coli O157, while in the 5–12 days group of clinically healthy pigs the detection rate was 20.0% and in piglets with signs of diarrhea 44.5%. On 12th day the average weight of sick piglets was lower on 30.45% compared to the average weight of healthy individuals was found, and the losses among sick pigs at weaning on day 21 reached to 56%. The relationship between colibacteriosis piglets susceptibility with genotypes of FUT1 and MUC4 genes was identified. The studied population of pigs is unreliable for colibacteriosis, so a gene pool study for the presence of the desired colibacteriosis resistance genotypes of FUT1 and MUC4 marker genes, followed by selection of parental cross-breeding forms, should be included in the livestock reproduction program.

Rotavirus A shedding and HBGA host genetic susceptibility in a birth community-cohort, Rio de Janeiro, Brazil, 2014\u20132018

Recent studies have investigated whether the human histo-blood group antigen (HBGAs) could affect the effectiveness of the oral rotavirus vaccines, suggesting secretor positive individuals develop a more robust response. We investigated the Rotavirus A (RVA) shedding in association with the host susceptibility profile in children from a birth community-cohort in Rio de Janeiro, Brazil, from 2014 to 2018. A total of 132 children were followed-up between 0 to 11-month-old, stool samples were collected before/after the 1st/2nd RV1 vaccination doses and saliva samples were collected during the study. RVA shedding was screened by RT-qPCR and G/P genotypes determined by multiplex RT-PCR and/or Sanger nucleotide sequencing. The sequencing indicated an F167L amino acid change in the RV1 VP8* P[8] in 20.5% of shedding follow-ups and these mutant subpopulations were quantified by pyrosequencing. The HBGA/secretor status was determined and 80.3% of the children were secretors. Twenty-one FUT2 gene SNPs were identified and two new mutations were observed. The mutant F167L RV1 VP8* P[8] was detected significantly more in Le (a+b+) secretors (90.5%) compared to non-secretors and even to secretors Le (a−b+) (9.5%). The study highlights the probable association between RV1 shedding and HBGAs as a marker for evaluating vaccine strain host susceptibility.