Systems-wide analyses of mucosal immune responses to<i>Helicobacter pylori</i>at the interface between pathogenicity and symbiosis

Kronsteiner, Barbara; Bassaganya‐Riera, Josep; Philipson, Casandra; Viladomiu, Monica; Carbo, Adria; Abedi, Vida; Hontecillas, Raquel

doi:10.1080/19490976.2015.1116673

Cited by 40 publications

(43 citation statements)

References 153 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, emerging clinical and epidemiological data support the theory that H. pylori might also be a beneficial commensal organism and its disappearance has been linked to increased incidence of diseases like asthma or IBD (53, 54). Indeed, H. pylori ’s ability to establish life-long chronic colonization of the gastric mucosal niche has been linked to the induction of potent regulatory responses that dampen effector mechanisms of bacterial eradication, although the induction of these responses has been attributed mainly to the modulation of DC, as opposed to macrophages (55–57). In any case, the mechanisms underlying the induction of these protective responses are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

Cooperation of Gastric Mononuclear Phagocytes with Helicobacter pylori during Colonization

Viladomiu

Bassaganya‐Riera

Tubau-Juni

et al. 2017

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

Helicobacter pylori, the dominant member of the human gastric microbiota, elicits immunoregulatory responses implicated in protective versus pathological outcomes. To evaluate the role of macrophages during infection, we employed a system with a shifted pro-inflammatory macrophage phenotype by deleting PPARγ in myeloid cells, and found a 5 to 10-fold decrease in gastric bacterial loads. Higher levels of colonization in wild-type (WT) mice were associated with increased presence of mononuclear phagocytes (MNPs) and in particular with the accumulation of CD11b+F4/80hiCD64+CX3CR1+ macrophages in the gastric lamina propria. Depletion of phagocytic cells by clodronate liposomes in WT resulted in a reduction of gastric H. pylori colonization compared to non-treated mice. PPARγ-deficient and macrophage-depleted mice presented decreased IL-10-mediated myeloid and T cell regulatory responses early post-infection. IL-10 neutralization during H. pylori infection led to increased IL-17-mediated responses and increased neutrophil accumulation at the gastric mucosa. In conclusion, we report the induction of IL-10-driven regulatory responses mediated by CD11b+F4/80hiCD64+CX3CR1+ MNPs that contribute to maintaining high levels of H pylori loads in the stomach by modulating effector T cell responses at the gastric mucosa.

show abstract

Section: Discussionmentioning

confidence: 99%

Cooperation of Gastric Mononuclear Phagocytes with Helicobacter pylori during Colonization

Viladomiu

Bassaganya‐Riera

Tubau-Juni

et al. 2017

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

show abstract

“…The gut microbiome and the mechanism of surgical infection e15 Unfortunately, the H. pylori story was wholly dismissive of the potential role of the microbiome in the pathogenesis of ulcer disease that is now coming to light 1 . The presence of an abundant and diverse microbiome within the stomach and duodenum may be an unrecognized defence factor in the pathogenesis of ulcer disease 2 .…”

Section: Introductionmentioning

confidence: 99%

The gut microbiome and the mechanism of surgical infection

Alverdy

Hyoju

Weigerinck

et al. 2017

British Journal of Surgery

View full text Add to dashboard Cite

Background: Since the very early days of surgical practice, surgeons have recognized the importance of considering that intestinal microbes might have a profound influence on recovery from surgical diseases such as appendicitis and peritonitis. Although the pathogenesis of surgical diseases such as cholelithiasis, diverticulosis, peptic ulcer disease and cancer have been viewed as disorders of host biology, they are emerging as diseases highly influenced by their surrounding microbiota.Methods: This is a review of evolving concepts in microbiome sciences across a variety of surgical diseases and disorders, with a focus on disease aetiology and treatment options.Results: The discovery that peptic ulcer disease and, in some instances, gastric cancer can now be considered as infectious diseases means that to advance surgical practice humans need to be viewed as superorganisms, consisting of both host and microbial genes. Applying this line of reasoning to the ever-ageing population of patients demands a more complete understanding of the effects of modern-day stressors on both the host metabolome and microbiome.

show abstract

“…Now, after penetration, the phagocytosis evasion mechanisms are initiated by H. pylori cells. Virulent strains of H. pylori (vacA positive and cagA positive) are highly resistant for phagocytosis as compared to the nonvirulent H. pylori strains . Stockpiling of H. pylori can stimulate the production of megasomes.…”

Section: Ureasementioning

confidence: 99%

“…Virulent strains of H. pylori (vacA positive and cagA positive) are highly resistant for phagocytosis as compared to the nonvirulent H. pylori strains. 80,81 Stockpiling of H. pylori can stimulate the production of megasomes. Delayed phagocytosis by producing megasomes could be one of the reasons to extend the survival duration of H. pylori for better response against immune system.…”

Section: Gastrointestinal Immunological Responses After Infection Omentioning

confidence: 99%

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Gupta

Maurya

Verma

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

Helicobacter pylori and humans have one of the most complex relationships in nature. How a bacterium manages to live in one of the harshest and hostile environments is a topic of unraveling mysteries. H. pylori is a prevalent species and it colonizes the human gut of more than 50% of the world population. It infects the epithelial region of antrum and persists there for a long period. Over the time of evolution, H. pylori has developed complex strategies to extend the degree of inflammation in gastric mucosa. H. pylori needs specific adaptations for initial colonization into the host environment like helical shape, flagellar movement, chemotaxis, and the production of urease enzyme that neutralizes acidic environment of the stomach. There are several factors from the bacterium as well as from the host that participate in these complex interactions. On the other hand, to establish the persistent infection, H. pylori escapes the immune system by mimicking the host antigens. This pathogen has the ability to dodge the immune system and then persist there in the form of host cell, which leads to immune tolerance. H. pylori has an ability to manipulate its own pathogen‐associated molecular patterns, which leads to an inhibition in the binding with specific pattern recognition receptors of the host to avoid immune cell detection. Also, it manipulates the host metabolic homeostasis in the gastric epithelium. Besides, it has several genes, which may get involved in the acquisition of nutrition from the host to survive longer in the host. Due to the persistence of H. pylori, it causes chronic inflammation and raises the chances of gastric cancer. This review highlights the important elements, which are certainly responsible for the persistence of H. pylori in the human host.

show abstract

Systems-wide analyses of mucosal immune responses toHelicobacter pyloriat the interface between pathogenicity and symbiosis

Cited by 40 publications

References 153 publications

Cooperation of Gastric Mononuclear Phagocytes with Helicobacter pylori during Colonization

Cooperation of Gastric Mononuclear Phagocytes with Helicobacter pylori during Colonization

The gut microbiome and the mechanism of surgical infection

Unraveling the factors and mechanism involved in persistence: Host‐pathogen interactions in Helicobacter pylori

Contact Info

Product

Resources

About