Evaluation of the Clinical Significance ofhomB,a Novel Candidate Marker ofHelicobacter pyloriStrains Associated with Peptic Ulcer Disease

Abstract

homB can be considered a comarker of H. pylori strains associated with PUD. Moreover, results strongly suggest that HomB is involved in the inflammatory response and in H. pylori adherence, constituting a novel putative virulence factor.

homB Status of Helicobacter pylori as a Novel Marker To Distinguish Gastric Cancer from Duodenal Ulcer

“…Recent studies suggested that there was a close association between the presence of the homB gene and interleukin-8 secretion from human gastric epithelial cells and that the number of H. pylori isolates binding to gastric cells was related to the number of homB copies present (15). Moreover, the authors proposed that the presence of the homB gene was significantly associated with PUD in Portuguese children and adults less than 40 years of age and that it may be a new H. pylori virulence factor (15,16). However, there is no study for the association between the homB gene and H. pylori-related diseases in other countries.…”

Interleukin‐8 gene regulation in epithelial cells by Vibrio cholerae: role of multiple promoter elements, adherence and motility of bacteria and host MAPKs

“…Yersinia enterocolitica outer membrane protein invasin triggered IL-8 in intestinal epithelial cells [35]. The OMP coding gene of H. pyroli, involved in bacterial adherence contributes to the proinflammatory characteristics of H. pyroli and increased incidence of peptic ulcer diseases [36]. We hypothesize that the reduction in IL-8 secretion obtained with the OmpU insertional mutant OMPUN could be due to alterations in the adherence of bacteria.…”

Helicobacter pylori—Associated Dyspepsia in Paediatrics

“…Nevertheless, H. pylori-associated peptic ulcer disease may also occur shortly after infection in childhood [4][5][6][7][8]. This rare event may be due to more virulent strains [9][10][11][12][13][14][15][16], and/or more predisposed subjects [17][18][19]. The two forms of H. pylori-associated peptic ulcers, i.e., gastric ulcer and duodenal ulcers, are divergent in prevalence and physiopathology, but both cause considerable patients' morbidity entailing high annual costs of treatment [93].…”

“…Indeed, H. pylori paediatric infection may be regarded as a privileged natural study model of the interaction of this bacterium with human host, as the child is usually not exposed to injurious factors as is the adult and represents a different stage of H. pylori infection in a immunologically maturing host. Comparative genomic studies of the rare paediatric ulcerogenic H. pylori strains and of the non-ulcerogenic strains show a distinctive genotype virulence pattern, suggesting a potential pathogenic role for new markers [9][10][11][12][13][14][15]. Two putative virulence determinants are associated with peptic ulceration, mostly duodenal ulcer, in children and with other H. pylori-virulence factors: jhp0562, involved in lipopolysaccharide biosynthesis and in the regulation of Lewis antigen expression [13]; and homB, a putative outer membrane protein, involved in bacterial adherence [9,11,12,14,15].…”

“…If often asymptomatic, the H. pylori-associated non-ulcer dyspepsia is clearly the strongest aetiological factor for severe gastric diseases that will develop late in adult life in a minority of infected patients, i.e., peptic ulcer disease, both gastric and duodenal ulcers, and gastric cancer, namely, adenocarcinoma and mucosa associated lymphoid tissue (MALT) lymphoma (reviewed in [3]). Peptic ulcer disease rarely occurs soon after H. pylori infection [4][5][6][7][8] that generally starts in childhood; this presumably reflects marked differences in the virulence [9][10][11][12][13][14][15][16] and/or in the susceptibility of young patients [17][18][19].…”