Helicobacter pylori colonization of the human gastric epithelium: A bug's first step is a novel target for us

Abstract

After Helicobacter pylori enters the stomach, three steps are vital for infection: (i) establishing colonization; (ii) evading host immunity; and (iii) invading gastric mucosa; the last step is what is associated with diverse outcomes. Urease activity and motility mediated by the flagella of H. pylori are important in harboring colonies beneath the gastric mucus in niches adjacent to the epithelium. Several putative adhesins attach the organism to the gastric epithelium and prompt the succeeding processes for evading host immunity and invading the mucosa. Successful colonization is thus the leading and critical step. From another point of view, this can be a novel target to control this common and important infection. This review summarizes the putative adhesins that influence the evasion of host immunity, and how these could determine different clinico-pathologic outcomes. The putative adhesins include the interplay between bacterial and host Lewis antigens (type I: Le a and Le b

Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer

“…In Taiwan, the H. pylori isolates have universal presence of genes in cag -PAI and expression of CagA [13-16]. On the basis of the semi-quantitative analysis of the translocated p-CagA bands in the western blots, the strains in this study have diverse intensity of p-CagA.…”

“…In contrast, in the eastern countries, such as in Taiwan, there is a nearly 100% prevalence of cagA-vacA-babA2 triple-positive H. pylori strains [13-15]. Moreover, most strains in East-Asia, and also Taiwan, encoded CagA contain EPIYA-ABD motif [16-18].…”

Inhibition of Helicobacter pylori growth and its colonization factors by Parthenium hysterophorus extracts

“…In this sense, several studies show that the binding of the bacteria is mediated by multiple adhesins (the most studied are BabA and SabA) and different receptors whose availability changes according to inflammation and glycan expression at the epithelial surface (Sheu et al, 2010). Up to now, it is not completely characterized the complex adherence-receptor network related to H. pylori infection.…”

Clinical relevance of the cagA, tnpA and tnpB genes in Helicobacter pylori

“…Infection rates range between 85-95% in developing countries and 30-50% in developed countries [1]. Colonization always results in acute gastritis and chronic gastritis when left untreated [2]. Additional complications such as gastric ulcers (GU), duodenal ulcers (DU), or gastric cancer (GC) may develop in some of these H. pylori infected patients [3].…”