pylori virulence

markers and found a high incidence of ca

pylori virulence

markers and found a high incidence of cagA and vacAs1 allele (in 66.1 and 91.7%, respectively) in asymptomatic children with H. pylori infection in a gastric cancer high risk area in Columbia. Authors concluded that this could be a contributing factor for the high incidence of gastric cancer in adults in this area. Moreover, these noninvasive assays could be useful for the screening of asymptomatic and symptomatic individuals. The virulence role of iceA allele was not clearly demonstrated until recently when a meta-analysis involving 50 relevant studies confirmed the importance of iceA1 allele in the development of peptic ulcer disease (PUD), especially duodenal ulcer [2]. On the other hand, connection between iceA allele and gastric cancer was not confirmed [2]. Lewis (Le) blood-group epitopes LDK378 on the surface of H. pylori mimic structures present on human gastric surfaces and could be implicated in adverse autoimmune reactions of the host. Most studies in adults found that the SCH727965 nmr majority of the H. pylori strains express type 2 Lex

and/or Ley antigens, while pediatric isolates have the tendency to express also type 1 Leb antigen [3]. Moreover, pediatric isolates have overwhelming presence of α1,6-glucan, yet another phenotypic characteristic that facilitates colonization and contributes to the antigenic diversity of H. pylori Plasmin surface [3]. For better understanding of the host immune response to H. pylori infection, Freire De Melo et al.[4] compared gastric level of Th17- and Treg-associated cytokines in children and adults. In children, Treg-cell differentiation was more predominant and might be responsible for the increased susceptibility of pediatric patients to infection and for lower degree of mononuclear and polymorphonuclear infiltration of gastric mucosa. Considering host’s genetics, in particular polymorphism of IL-1 gene cluster, study in children revealed the IL-1B-511TT/31CC genotype as a risk factor for more severe gastrointestinal

disease [5]. Moreover, the proteome of H. pylori strains isolated from children with PUD differs substantially from the proteome of H. pylori isolated from children with non-ulcer dyspepsia [6]. The pediatric ulcerogenic H. pylori strains share a particular proteome profile that, in addition to the well-established virulence factors, provides bacteria with better motility, increased antioxidant defense mechanisms, and metabolism that favors the biosynthesis of aromatic amino acids [6]. Evolving proteomic technologies, together with new information regarding the bacterial and host genotype, may result in more precise detection of patients with the higher risk of severe disease. Over the last decade, the prevalence of H. pylori in the developed world has steadily decreased. Interestingly, a decrease in the incidence was not reported in all studies.

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