Background The homB gene is a Helicobacter pylori disease-marker candidate, strongly associated with peptic ulcer disease, while homA, its paralogue gene with 90% sequence identity, is correlated with non-ulcer dyspepsia. strains. Analysis of homB and homA sequences revealed diversity regarding the number of copies and their genomic localization, with East Asian and Western strains presenting different genotypes. Moreover, homB and homA sequence analysis suggests regulation buy Droxinostat by phase variation. It also indicates possible recombination events, leading to gene duplication or homB/homA conversion which may as well be implicated in the regulation of these genes. Phylogenetic reconstruction of homB and homA revealed buy Droxinostat clustering according to the geographic origin of strains. Allelic diversity in the middle region of the genes was observed for both homB and homA, although there was no correlation between buy Droxinostat any allele and disease. For each gene, a dominant worldwide allele was detected, suggesting that homB/homA allelic variants were independent of the geographical origin of the strain. Moreover, all alleles were demonstrated to be expressed in vivo. Conclusion Overall, these results suggest that homB and homA genes are good candidates to be part of the pool of H. pylori OMPs implicated in host-bacteria interface and also contributing to the generation of antigenic variability, and thus involved in H. pylori persistence. Background H. pylori infection is implicated in the development of several gastroduodenal diseases, ranging from chronic active gastritis and dyspepsia to peptic ulcer disease (PUD), and associated with an increased risk for gastric cancer . The virulence of the infecting strain influences the severity of the clinical outcome, and disease associations have been proposed for the cag pathogenicity island (PAI), vacA and several genes encoding outer membrane proteins (OMP) [2-7]. Indeed, bacterial factors which modulate interactions with human cells, such as OMPs, have been involved in the pathophysiology of the infection caused by H. pylori. These proteins can contribute to the colonization and persistence of H. pylori, as well as influence the disease process [5-7]. PUD usually occurs after a long-term H. pylori infection. However, the disease can develop earlier, and rare cases have been observed in children, suggesting that the H. pylori strains involved are more virulent. Recently, a novel virulence-associated OMP-coding gene, homB, was identified in the genome of a H. pylori strain isolated from a five-year old child with a duodenal ulcer . The homB gene was associated with an increased risk of PUD as well Rabbit polyclonal to Caspase 9.This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family. as with the presence of other H. pylori disease-related genes: cagA, babA, vacAs1, hopQI and functional oipA [8-10]. Several H. pylori strains carry a paralogue of homB, the homA gene, which presents more than 90% identity to homB . Interestingly, homA was more frequently found in strains isolated from non-ulcer dyspepsia (NUD), and was associated with the less virulent H. pylori genotypes i.e. cagA-negative and babA-negative, vacAs2, hopQII and a non-functional oipA gene [9,10]. Both homB and homA genes can be found as a single or double-copy in the H. pylori genome, or alternatively a copy of each gene can be present within a genome, in two conserved loci . When present as a single copy, the gene always occupies the HP0710/jhp0649 locus, while when present as a double-copy, homA and homB occupy indifferently the HP0710/jhp0649 or jhp0870 loci , according to the numbering of the 26695 and J99 strains, respectively [12,13]. Furthermore, among all possible homB and homA combinations, the genotype the most significantly associated with PUD was the double-copy of homB, while a single copy of homA was the genotype the most associated with NUD [9,10]. In vitro studies revealed that the HomB protein is expressed as an OMP and is antigenic in humans. Moreover, HomB induces activation of interleukin-8 secretion and is involved in adherence to human gastric epithelial cells; these two phenomena being more pronounced in strains carrying the homB double-copy genotype . Taken together, these data suggest that homB gene is.