BACKGROUND: Helicobacter pylori is a causative agent of gastritis, and H. pylori infection is thought to be correlated with iron-deficiency anemia (IDA) at puberty. The H. pylori feoB gene product, a high-affinity ferrous iron transporter, plays a central role in iron acquisition and virulence. This study was undertaken to analyze H. pylori feoB status according to clinical data, including antral gastritis with or without IDA. METHODS: Fourteen H. pylori-positive patients aged from 10 to 18 years were categorized into subgroups based on the presence or absence of IDA. Eight patients were diagnosed as having IDA; the other six showed normal hematological findings. Genomic DNA was isolated from H. pylori cultured from each gastric biopsy specimen. Five sets of primers were used for the PCR amplification of the feoB gene. Linking and sequencing of PCR products generated the feoB region, which was 1.93 kb in size. The feoB gene sequences of H. pylori J99 and 26695 were compared with the clinical strains, and the sequences of feoB regions in the IDA (+) and (-) groups were compared. RESULTS: Sequence analysis of the complete coding region of the feoB gene revealed 16 sites of polymorphism or mutation. Among these, three polymorphisms (E/T254A, I263V, and K511Q) were indigenous to the Korean clinical strains. Although statistically significant differences were observed at four sites (K127T, A273S/P, I438V and I441T) between IDA (+) and (-), the number of specimens was too low to assess the significance of the differences. CONCLUSION: The four polymorphisms of the feoB gene observed appear to be related to the clinical phenotype of IDA, but the relation is unclear because of the small number of strains studied. Further studies are required to confirm a correlation between IDA and H. pylori infection.
BACKGROUND:Helicobacter pylori is a causative agent of gastritis, and H. pyloriinfection is thought to be correlated with iron-deficiency anemia (IDA) at puberty. The H. pylori feoB gene product, a high-affinity ferrous iron transporter, plays a central role in iron acquisition and virulence. This study was undertaken to analyze H. pylori feoB status according to clinical data, including antral gastritis with or without IDA. METHODS: Fourteen H. pylori-positive patients aged from 10 to 18 years were categorized into subgroups based on the presence or absence of IDA. Eight patients were diagnosed as having IDA; the other six showed normal hematological findings. Genomic DNA was isolated from H. pylori cultured from each gastric biopsy specimen. Five sets of primers were used for the PCR amplification of the feoB gene. Linking and sequencing of PCR products generated the feoB region, which was 1.93 kb in size. The feoB gene sequences of H. pylori J99 and 26695 were compared with the clinical strains, and the sequences of feoB regions in the IDA (+) and (-) groups were compared. RESULTS: Sequence analysis of the complete coding region of the feoB gene revealed 16 sites of polymorphism or mutation. Among these, three polymorphisms (E/T254A, I263V, and K511Q) were indigenous to the Korean clinical strains. Although statistically significant differences were observed at four sites (K127T, A273S/P, I438V and I441T) between IDA (+) and (-), the number of specimens was too low to assess the significance of the differences. CONCLUSION: The four polymorphisms of the feoB gene observed appear to be related to the clinical phenotype of IDA, but the relation is unclear because of the small number of strains studied. Further studies are required to confirm a correlation between IDA and H. pyloriinfection.
Authors: Melanie J Thomson; D Mark Pritchard; Sally A Boxall; Abdul A Abuderman; Jonathan M Williams; Andrea Varro; Jean E Crabtree Journal: PLoS One Date: 2012-11-19 Impact factor: 3.240