The aim of this work was to investigate the FUT2 gene, the secretor status and the expression of CD44 protein in epithelial cells obtain from saliva and urine samples from patients with urogenital tumours. We studied ...The aim of this work was to investigate the FUT2 gene, the secretor status and the expression of CD44 protein in epithelial cells obtain from saliva and urine samples from patients with urogenital tumours. We studied 104 subjects. Half of them had urogenital tumours, while the other half was the healthy control group. We determined the secretor status in saliva with the haemagglutination inhibition technique. We analyzed the FUT2 polymorphism by allele specific oligonucleotide–polymerase chain reaction (ASO-PCR) with specific primers for the G428 allele and the wild type allele of FUT2 gene. We found higher intensity of urogenital disease in the non-secretor group (OR = 3.44). In contrast with the healthy population, 51.6% of the patients with potential malignant urogenital lesions and cancerous lesions were non-secretors. We also investigate by confocal microscopy, the expression of CD44 protein in epithelial cells obtained from urine samples from these patients. The results obtained also showed fluorescence corresponding to the presence of CD44 protein in samples from patients diagnosed with cancer. Our study suggests that the lack of wild type FUT2 gene and a nonsecretor status appear to be an associated risk marker for the development of urogenital tumors. Several mechanisms, based on the properties of CD44 as the major hyaluronan CD44 in cell carcinomas receptor, have been proposed to explain the role of elevated CD44 expression during tumour development and progression. CD44 might be a good candidate as a predictor of prognosis in this group of cancers.展开更多
Background. Secretor (Se) and Lewis (Le) genes are involved in the synthesis of Lewis b (Leb) and type I antigens throughout the body, especially in the epithelial cells of gastric mucosa. Helicobacter pylori can atta...Background. Secretor (Se) and Lewis (Le) genes are involved in the synthesis of Lewis b (Leb) and type I antigens throughout the body, especially in the epithelial cells of gastric mucosa. Helicobacter pylori can attach to the gastric epithelial cells with the blood group antigen binding adhesin, which binds to Leb or H type I carbohydrate structures. In a previous study, a marked association between H. pylori seropositivity and polymorphism of the Se and Le genes was observed among Japanese outpatients of a gastroenterology clinic. The present work aims to investigate the associations between Se and Le gene polymorphisms and H. pylori infection among Japanese Brazilians. Methods. The subjects consisted of 942 healthy volunteer Japanese Brazilians, who were tested for the presence of anti H. pylori IgG antibodies and genotyped for Se and Le polymorphisms. Results. The sex age adjusted odds ratios (aORs) for H. pylori seropositivity were 0.99 for the Sese genotype relative to the SeSe genotype (95%confidence interval , 0.73-1.33), and 1.03 for sese relative to SeSe (95%CI, 0.71-1.48). On the other hand, the aOR for the subjects with the le allele (Lele or lele) relative to the LeLe genotype was 1.48 (95%CI, 1.07-1.79). When the Se and Le genotypes were analyzed in combination according to risk group, no statistically significant association was observed. Conclusions. These results are inconsistent with previous work and may have been modulated by an external factor or some other unidentified factor. Japanese Brazilians are geno typically the same as Japanese, but their lifestyle is adapted to that of Brazil. Further investigations are necessary to clarify this influence on susceptibility to H. pylori infection.展开更多
The composition and the diversity of the gut microbiome play a major role in the health and well-being of humans beginning at birth.The impact of the diet on the structure and the function of the gut microbiome is evi...The composition and the diversity of the gut microbiome play a major role in the health and well-being of humans beginning at birth.The impact of the diet on the structure and the function of the gut microbiome is evident by the changes in the gut microbiome concurrent with the transition from human milk to solid food.Complex oligosaccharides contained in milk are essential nutrients for commensal microbes in the infant gut.The most important commensal bacterium in the infant gut,bifidobacterium,requires a1,2 fucosylated oligosaccharides for growth.Because not all humans are able to secrete a1,2 fucosylated oligosaccharides into milk,the gut microbiome of infants and bifidobacteria,in particular,vary considerably between‘secretors’and‘non-secretors’.A paucity of a1,2 fucosylated oligosaccharides and bifidobacteria in the gut of infants may be associated with poor health.展开更多
The FUT2 loss-of-function mutations are highly prevalent and are associated with inflammatory bowel disease(IBD).To investigate the impact of FUT2 loss-of-function mutation on the gut microbiota in patients with IBD,8...The FUT2 loss-of-function mutations are highly prevalent and are associated with inflammatory bowel disease(IBD).To investigate the impact of FUT2 loss-of-function mutation on the gut microbiota in patients with IBD,81 endoscopically confirmed IBD patients were genotyped and divided into 3 groups:homozygous for functional FUT2 genes(SeSe),with one copy of non-functional FUT2 gene(Sese),or homozygous for non-functional FUT2 genes(sese).Escherichia,which attaches to fucosylated glycoconjugates,was the only abundant genus exhibiting decreased abundance in sese patients.Compared with SeSe or Sese patients,sese patients exhibited higher abundance in CD8+inducing Alistipe and Phascolarctobacterium and Th17 inducing Erysipelotrichaceae UCG-003.Counter-intuitively,butyrate-producing bacteria were more abundant in sese patients.Consistently,metabolomics analysis found higher levels of butyrate in sese patients.Our data support the hypothesis that FUT2 loss-of-function mutation participates in the IBD pathogenesis by decreasing binding sites for adherent bacteria and thus altering the gut microbiota.Decreased abundances of adherent bacteria may allow the overgrowth of bacteria that induce inflammatory T cells,leading to intestinal inflammation.As FUT2 loss-of-function mutations are highly prevalent,the identification of T cell inducing bacteria in sese patients could be valuable for the development of personalized microbial intervention for IBD.展开更多
文摘The aim of this work was to investigate the FUT2 gene, the secretor status and the expression of CD44 protein in epithelial cells obtain from saliva and urine samples from patients with urogenital tumours. We studied 104 subjects. Half of them had urogenital tumours, while the other half was the healthy control group. We determined the secretor status in saliva with the haemagglutination inhibition technique. We analyzed the FUT2 polymorphism by allele specific oligonucleotide–polymerase chain reaction (ASO-PCR) with specific primers for the G428 allele and the wild type allele of FUT2 gene. We found higher intensity of urogenital disease in the non-secretor group (OR = 3.44). In contrast with the healthy population, 51.6% of the patients with potential malignant urogenital lesions and cancerous lesions were non-secretors. We also investigate by confocal microscopy, the expression of CD44 protein in epithelial cells obtained from urine samples from these patients. The results obtained also showed fluorescence corresponding to the presence of CD44 protein in samples from patients diagnosed with cancer. Our study suggests that the lack of wild type FUT2 gene and a nonsecretor status appear to be an associated risk marker for the development of urogenital tumors. Several mechanisms, based on the properties of CD44 as the major hyaluronan CD44 in cell carcinomas receptor, have been proposed to explain the role of elevated CD44 expression during tumour development and progression. CD44 might be a good candidate as a predictor of prognosis in this group of cancers.
文摘Background. Secretor (Se) and Lewis (Le) genes are involved in the synthesis of Lewis b (Leb) and type I antigens throughout the body, especially in the epithelial cells of gastric mucosa. Helicobacter pylori can attach to the gastric epithelial cells with the blood group antigen binding adhesin, which binds to Leb or H type I carbohydrate structures. In a previous study, a marked association between H. pylori seropositivity and polymorphism of the Se and Le genes was observed among Japanese outpatients of a gastroenterology clinic. The present work aims to investigate the associations between Se and Le gene polymorphisms and H. pylori infection among Japanese Brazilians. Methods. The subjects consisted of 942 healthy volunteer Japanese Brazilians, who were tested for the presence of anti H. pylori IgG antibodies and genotyped for Se and Le polymorphisms. Results. The sex age adjusted odds ratios (aORs) for H. pylori seropositivity were 0.99 for the Sese genotype relative to the SeSe genotype (95%confidence interval , 0.73-1.33), and 1.03 for sese relative to SeSe (95%CI, 0.71-1.48). On the other hand, the aOR for the subjects with the le allele (Lele or lele) relative to the LeLe genotype was 1.48 (95%CI, 1.07-1.79). When the Se and Le genotypes were analyzed in combination according to risk group, no statistically significant association was observed. Conclusions. These results are inconsistent with previous work and may have been modulated by an external factor or some other unidentified factor. Japanese Brazilians are geno typically the same as Japanese, but their lifestyle is adapted to that of Brazil. Further investigations are necessary to clarify this influence on susceptibility to H. pylori infection.
文摘The composition and the diversity of the gut microbiome play a major role in the health and well-being of humans beginning at birth.The impact of the diet on the structure and the function of the gut microbiome is evident by the changes in the gut microbiome concurrent with the transition from human milk to solid food.Complex oligosaccharides contained in milk are essential nutrients for commensal microbes in the infant gut.The most important commensal bacterium in the infant gut,bifidobacterium,requires a1,2 fucosylated oligosaccharides for growth.Because not all humans are able to secrete a1,2 fucosylated oligosaccharides into milk,the gut microbiome of infants and bifidobacteria,in particular,vary considerably between‘secretors’and‘non-secretors’.A paucity of a1,2 fucosylated oligosaccharides and bifidobacteria in the gut of infants may be associated with poor health.
基金supported by Guangdong Province“Pearl River Talent Plan”Innovation and Entrepreneurship Team Project 2019ZT08Y464(to L.Z.)the National Natural Science Foundation of China 81770571(to L.Z.),82000536(to N.J.)+2 种基金National Postdoctoral Program for Innovative Talents of China BX20190393(to N.J.)China Postdoctoral Science Foundation 2019M663252(to N.J.)Fundamental Research Funds for the Central Universities 19ykzd01(to L.Z.),and 20kypy07(to N.J.)。
文摘The FUT2 loss-of-function mutations are highly prevalent and are associated with inflammatory bowel disease(IBD).To investigate the impact of FUT2 loss-of-function mutation on the gut microbiota in patients with IBD,81 endoscopically confirmed IBD patients were genotyped and divided into 3 groups:homozygous for functional FUT2 genes(SeSe),with one copy of non-functional FUT2 gene(Sese),or homozygous for non-functional FUT2 genes(sese).Escherichia,which attaches to fucosylated glycoconjugates,was the only abundant genus exhibiting decreased abundance in sese patients.Compared with SeSe or Sese patients,sese patients exhibited higher abundance in CD8+inducing Alistipe and Phascolarctobacterium and Th17 inducing Erysipelotrichaceae UCG-003.Counter-intuitively,butyrate-producing bacteria were more abundant in sese patients.Consistently,metabolomics analysis found higher levels of butyrate in sese patients.Our data support the hypothesis that FUT2 loss-of-function mutation participates in the IBD pathogenesis by decreasing binding sites for adherent bacteria and thus altering the gut microbiota.Decreased abundances of adherent bacteria may allow the overgrowth of bacteria that induce inflammatory T cells,leading to intestinal inflammation.As FUT2 loss-of-function mutations are highly prevalent,the identification of T cell inducing bacteria in sese patients could be valuable for the development of personalized microbial intervention for IBD.
