Helicobacter pylori Infection of the Gastric Mucosa

Raghavan, Sukanya; Holmgren, Jan; Svennerholm, Ann‐Mari

doi:10.1016/b978-0-12-415847-4.00051-3

Cited by 5 publications

(6 citation statements)

References 191 publications

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“…Helicobacter pylori infection in the stomach is a common cause of peptic ulcer disease and is a strong risk factor for the development of gastric adenocarcinoma. Infection is characterized by gastritis that remains chronic for decades, with an influx of immune cells such as dendritic cells (DCs), M1 and M2 macrophages, eosinophils, neutrophils and lymphocytes . The recruited immune cells secrete a range of pro‐inflammatory cytokines such as interleukin‐12p40 (IL‐12p40), IL‐1 β , tumour necrosis factor‐ α (TNF‐ α ), interferon‐ γ (IFN‐ γ ) and IL‐17A.…”

Section: Introductionmentioning

confidence: 99%

Induction of mucosal immune responses against Helicobacter pylori infection after sublingual and intragastric route of immunization

et al. 2016

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SummaryThere is a current lack of effective mucosal vaccines against major gastroenteric pathogens and particularly against Helicobacter pylori, which causes a chronic infection that can lead to peptic ulcers and gastric cancer in a subpopulation of infected individuals. Mucosal CD4 + T-cell responses have been shown to be essential for vaccine-induced protection against H. pylori infection. The current study addresses the influence of the adjuvant and site of mucosal immunization on early CD4 + T-cell priming to H. pylori antigens. The vaccine formulation consisted of H. pylori lysate antigens and mucosal adjuvants, cholera toxin (CT) or a detoxified double-mutant heat-labile enterotoxin from Escherichia coli (dmLT), which were administered by either the sublingual or intragastric route. We report that in vitro, adjuvants CT and dmLT induce up-regulation of proinflammatory gene expression in purified dendritic cells and enhance the H. pylori-specific CD4 + T-cell response including interleukin-17A (IL-

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Section: Introductionmentioning

confidence: 99%

Induction of mucosal immune responses against Helicobacter pylori infection after sublingual and intragastric route of immunization

et al. 2016

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“…HP colonization in gastric mucosa results the activation of innate and adaptive immune cells such as; neutrophils, dendritic cells, M1 and M2 macrophages, mast cells and T and B lymphocytes to the stomach where they secrete cytokines such as IL-1b, IL-6, TNF, IL-8, IFNc, and IL-17A; this generates a pro-inflammatory milieu that is characteristic of HP infection and the presence of chemokines, which help recruit neutrophils and APCs to the site of infection [44,45]. Recently, Tourani et al revealed that the cytokines TNF-a and IL-1b play a crucial role in the pathogenesis of PUD [10].…”

Section: Pathophysiology Of Pudmentioning

confidence: 99%

The role of toll-like receptors in peptic ulcer disease

Jin

Nepal

Gao

2021

Immunological Medicine

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Helicobacter pylori (HP) is the primary etiologic factor that induces events in the immune system that lead to peptic ulcers. Toll-like receptors (TLRs) are an important part of the innate immune system, as they play pivotal roles in pathogen-associated molecular pattern (PAMP) recognition of HP as well host-associated damage-associated molecular patterns (DAMPs). Recent advancements such as COX-2 production, LPS recognition through TLR2, CagL, and CagY protein of HP activating TLR5, TLR9 activation via type IV secretion system (T4SS) using DNA transfer, TLR polymorphisms, their adaptor molecules, cytokines, and other factors play a significant role in PUD. Thus, some novel PUD treatments including Chuyou Yuyang granules, function by TLR4/NF-jB signaling pathway suppression and TNF-a and IL-18 inhibition also rely on TLR signaling. Similarly glycyrrhetinic acid (GA) treatment activates TLR-4 in Ana-1 cells not via TRIF, but via MYD88 expression, which is significantly upregulated to cure PUD. Therefore, understanding TLR signaling complexity and its resultant immune modulation after host-pathogen interactions is pivotal to drug and vaccine development for other diseases as well including cancer and recent pandemic COVID-19. In this review, we summarize the TLRs and HP interaction; its pathophysiology-related signaling pathways, polymorphisms, and pharmaceutical approaches toward PUD.

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“…2 Natural infection does not induce protective immunity in a majority of infected individuals, and the infection can persist for decades with a mucosal infiltration of immune cells such as dendritic cells (DCs), macrophages, granulocytes and lymphocytes mediated by secreted cytokines and chemokines. 3,4 Protective immunity against H pylori infection can instead be induced by mucosal vaccination resulting in the reduction of bacterial load compared to sham-vaccinated mice. 5,6 Vaccine-induced reduction in bacterial load has been shown to largely depend on migration of CD4 + Th1 and Th17 cells, mast cells and neutrophils to the stomach mucosa but not CD8 + T cells or B cells.…”

Section: Introductionmentioning

confidence: 99%

“…The role of chronic H pylori infection and inflammation in the etiology of gastric cancer classifies H pylori a class I carcinogen, according to the World Health Organization . Natural infection does not induce protective immunity in a majority of infected individuals, and the infection can persist for decades with a mucosal infiltration of immune cells such as dendritic cells (DCs), macrophages, granulocytes and lymphocytes mediated by secreted cytokines and chemokines …”

Section: Introductionmentioning

confidence: 99%

The frequency of circulating integrin α4β7⁺ cells correlates with protection against Helicobacter pylori infection in immunized mice

et al. 2019

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BackgroundChronic Helicobacter pylori infection is the cause of peptic ulcers in a subpopulation of individuals and a risk factor for the development of gastric cancer. A vaccine against H pylori infection can prevent the acquisition of the infection and protect against reinfections. Clinical trials to date evaluating the efficacy of H pylori vaccines in human challenge models have shown moderate to poor protection with difficulties in predicting efficacy. Thus, while further studies are needed to design an effective vaccine, we also need to find relevant correlates for vaccine efficacy.ObjectiveTo find immune correlates to vaccine efficacy, the frequencies of neutrophils, eosinophils and inflammatory monocytes and CD4+ T‐cell memory and mucosa homing integrin α4β7+ cells were assessed by flow cytometry in the blood of mice after vaccination.Materials and Methods H pylori antigens and cholera toxin or the multiple mutant CT (mmCT) were administered via the sublingual (SL) and intragastric route (IG). The vaccinated mice were infected with H pylori strain SS1 bacteria, and colonization in the stomach and immune responses were evaluated.ResultsThe H pylori vaccine was effective in reducing bacterial load in the stomach of mice and enhancing immune responses compared to unvaccinated infection controls. In the blood of mice after SL or IG route of vaccination, we observed changes in frequencies of innate and adaptive immune cell subsets compared to infection controls. Remarkably, the frequency of circulating mucosal homing α4β7+CD4+ T cells after vaccination correlated with low bacterial load in the stomach of individual mice irrespective of the immunization route.ConclusionsOur study shows that the innate and adaptive immune cell subsets can be measured in the blood after vaccination and that increased frequency of α4β7+CD4+ in the blood after immunization could be used as a predictive marker for the efficacy of vaccine against H pylori infection.

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Helicobacter pylori Infection of the Gastric Mucosa

Cited by 5 publications

References 191 publications

Induction of mucosal immune responses against Helicobacter pylori infection after sublingual and intragastric route of immunization

Induction of mucosal immune responses against Helicobacter pylori infection after sublingual and intragastric route of immunization

The role of toll-like receptors in peptic ulcer disease

The frequency of circulating integrin α4β7⁺ cells correlates with protection against Helicobacter pylori infection in immunized mice

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Helicobacter pylori Infection of the Gastric Mucosa

Cited by 5 publications

References 191 publications

Induction of mucosal immune responses against Helicobacter pylori infection after sublingual and intragastric route of immunization

Induction of mucosal immune responses against Helicobacter pylori infection after sublingual and intragastric route of immunization

The role of toll-like receptors in peptic ulcer disease

The frequency of circulating integrin α4β7+ cells correlates with protection against Helicobacter pylori infection in immunized mice

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The frequency of circulating integrin α4β7⁺ cells correlates with protection against Helicobacter pylori infection in immunized mice