Abstract
Helicobacter pylori (H. pylori) carcinogenicity depends on three major factors: bacterial virulence constituents, environmental factors and host’s genetic susceptibility. The relationship between microenvironmental factors and H. pylori virulence factors are incontestable. H. pylori infection has a major impact on both gastric and colonic microbiota. The presence of non-H. pylori bacteria within the gastric ecosystem is particularly important since they might persistently act as an antigenic stimulus or establish a partnership with H. pylori in order to augment the subsequent inflammatory responses. The gastric ecosystem, i.e., microbiota composition in children with H. pylori infection is dominated by Streptoccocus, Neisseria, Rothia and Staphylococcus. The impairment of this ecosystem enhances growth and invasion of different pathogenic bacteria, further impairing the balance between the immune system and mucosal barrier. Moreover, altered microbiota due to H. pylori infection is involved in increasing the gastric T regulatory cells response in children. Since gastric homeostasis is defined by the partnership between commensal bacteria and host’s immune system, this review is focused on how pathogen recognition through toll-like receptors (TLRs—an essential class of pathogen recognition receptors—PRRs) on the surface of macrophages and dendritic cells impact the immune response in the setting of H. pylori infection. Further studies are required for delineate precise role of bacterial community features and of immune system components.
Highlights
IntroductionPublisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations
Since gastric homeostasis is defined by the partnership between commensal bacteria and host’s immune system, this review is focused on how pathogen recognition through toll-like receptors (TLRs—an essential class of pathogen recognition receptors—Pathogen recognition receptors (PRRs)) on the surface of macrophages and dendritic cells impact the immune response in the setting of H. pylori infection
Studies performed on mice pointed out that gastric commensal bacteria have the ability to accelerate the inflammation caused by H. pylori, increasing the risk of carcinogenesis [47]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. H. pylori is a well-defined microaerophilic, Gram-negative bacterium that usually colonizes the human gastric mucosa during childhood and it might result in long-life inflammation and subsequent development of a wide spectrum of gastropathies like chronic gastritis, peptic ulcer disease and even certain types of malignant disorders [12,13]. A study performed by Cortes-Marquez et al concluded that the expression of certain types of miRNA might indicate the severity and the chronicity of the disease pointing out that the overexpression of miRNA-155 and miRNA-146a are associated with the persistence and outcome of H. pylori infection [31]. H. pylori binding avidity is definitely another sine qua non condition for the severity and persistence of this infection since the strains identified in children with peptic ulcer disease were shown to express a higher binding avidity as compared to those encountered in pediatric patients with non-ulcer dyspeptic symptoms [24]. H. pylori infection has a major impact on both gastric and colonic microbiota and several studies have assessed the interaction between this infection and the diversity of bacteria colonizing the gastrointestinal tract
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