<i>Helicobacter pylori</i> Infection and Gastric Dysbiosis: Can Probiotics Administration Be Useful to Treat This Condition?

Bruno, G; Rocco, Giulia; Zaccari, Piera; Porowska, Barbara; Mascellino, Maria Teresa; Severi, Carola

doi:10.1155/2018/6237239

Cited by 30 publications

(30 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…effects of Hp-induced DCs in the DC/CD4 + T-cell co-cultures by downregulation of IL-10 production, induction of IL-12p70 and IFN-γ levels, and decreased Treg generation. These observations may confirm the results of previous studies on the role of microbiota composition in resistance against Hp infection 43. The fact that only the Hp-antagonistic LAB strain (Lr) exerted this effect points out the need for testing more LAB strains as a potentially useful concomitant component of the standard eradication therapy.…”

supporting

confidence: 87%

Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

et al. 2019

View full text Add to dashboard Cite

Background The mechanisms of downregulation of protective immunity against Helicobacter pylori (Hp) infection strongly depend on dendritic cell (DC)‐induced T‐lymphocyte differentiation pattern. Lactic acid bacteria (LAB) strains can modulate Hp‐induced immunoresponse by changes in DC activation profiles. Here, we want to find out if the LAB‐pulsed DCs will change Hp‐induced T‐cell responsiveness patterns. Materials and Methods The naive peripheral CD4+ T cells were co‐cultured with Hp CagA + pulsed monocyte‐derived DCs (DC/CD4+ T cell) in the presence/absence of the feces‐derived probiotics: antagonistic or non‐antagonistic to Hp (Lactobacillus rhamnosus 900, Lr, Lactobacillus paracasei 915, Lp, respectively), as assessed by the agar slab method. The regulatory T‐cell (Treg) population was assessed by flow cytometry, and IFN‐γ, IL‐12p70, IL‐10, and IL‐17A levels were evaluated by ELISA method. Results The Hp‐pulsed DC/CD4+ T‐cell co‐cultures were characterized by high IL‐10, decreased IL‐12p70 and IFN‐γ levels, and elevated Treg population. In contrast, Lr‐pulsed DC/CD4+ T‐cell co‐cultures expressed low IL‐10, high IL‐12p70 and IFN‐γ levels and declined Treg population; this responsiveness pattern was not changed by Hp. The responsiveness pattern of the Lp/Hp‐pulsed DC/CD4+ T‐cell co‐cultures did not differ from those pulsed with Hp alone. Conclusion In contrast to Lp, Lr probiotic strain overcomes Hp‐mediated immune profile in the DC/T‐cell co‐cultures toward Th1 pattern and limited generation of Tregs in vitro. Lr may therefore be used as a component of anti‐Hp treatment.

show abstract

supporting

confidence: 87%

Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

et al. 2019

View full text Add to dashboard Cite

show abstract

“…The gastric colonization pattern is mainly based on Bacteroidetes and Firmicutes. Streptococcus strains predominate in the gastric microbiota, beside Prevotella and Veillonella [63]. It has been shown that PPIs chronic administration was associated to several adverse events as increased bacterial concentration and translocation and gastric stasis [64].…”

Section: The Influence Of Ppis On the Gut Microbiotamentioning

confidence: 99%

Proton-Pump Inhibitors in Adults and Pediatric Patients: Use and Abuse

Belei¹,

Amăricăi²,

Iacob³

et al. 2020

Rev. Chim.

View full text Add to dashboard Cite

Proton-Pump Inhibitors (PPIs) represent the major therapeutic tool of gastric acid-related disorders in adults and pediatric patients. The proton pump must be activated before the PPI is cleared from the circulation in order to effectively inhibit the H/K ATPase. This is related to time to reach maximum concentration, the absorption and elimination rate of the drug. All these features are modulated by age and genetics. Prolonged inhibition of gastric acid secretion may cause hypergastrinemia and enterochromaffin-like-cell hyperplasia, nutrients deficiency, necrotizing enterocolitis, atrophic gastritis, intestinal dysbiosis and digestive infections. These potential side effects have been described in adults, but pediatric studies are scarce. This review summarizes the pharmacodynamic features of PPIs and clarifies the side effects mechanisms of PPIs in children and adults.

show abstract

“…It has been proposed that Hp initially increases acid secretion and acid reflux, and decreases lower esophageal sphincter (LES) pressure, thereby increasing the risk of GERD and its related BE and EAC, whereas the subsequent Hp ‐induced atrophic gastritis might normalize this risk . However, hypochlorhydria, as a consequence of Hp ‐related atrophic gastritis, seems to induce alterations of the gastric microbiota (GM), namely gastric dysbiosis, which, beyond gastric pathologies, including gastric cancer, might also contribute to the BE−EAC sequence . In this regard, Campylobacter is among the most influential genera in Hp‐ induced atrophic gastritis specimens and gastric atrophy−related GM may be a significant contributor to gastric oncogenesis .…”

Section: Newer Considerationsmentioning

confidence: 99%

“…It seems, therefore, that Campylobacter species related to Hp‐ induced atrophic gastritis could be etiological agents of the chronic esophageal inflammation that results in EAC development . Moreover, the GM transformation from predominantly Gram‐positive to mostly Gram‐negative bacteria (including Hp ) suggests that dysbiosis is involved in the pathogenesis of the GERD−BE−EAC sequence …”

Section: Newer Considerationsmentioning

confidence: 99%

A perspective on risk factors for esophageal adenocarcinoma: emphasis on Helicobacter pylori infection

Kountouras

Doulberis

Papaefthymiou

et al. 2019

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Gastroesophageal reflux disease (GERD) and the increasing rate of its associated complications, including esophageal adenocarcinoma (EAC), has stimulated a plethora of studies attempting to evaluate provocative and protective factors. Helicobacter pylori (Hp) infection (Hp-I) was initially considered as a beneficial condition in GERD management based on rather limited data. Large-scale regional studies revealed an alternative approach, by suggesting a positive relationship between Hp-I and EAC development. Regarding pathophysiology, Hp-I induces gastric microbiota disturbances through hypochlorhydria and chronic inflammation, with a subsequent possible effect on the GERD−Barrett's esophagus (BE)−EAC cascade. Additionally, both direct effects on esophageal mucosa and indirect effects on known mechanisms of GERD, such as acid pocket and transient lower esophageal sphincter relaxation, remain to be elucidated. Hp contribution to carcinogenesis is related to oncogenic gastrin, cyclooxygenase-2, and prostaglandins; Ki-67 is also expressed and represents an index of BE-related malignancy. Moreover, Hp-I is vigorously suggested as a risk factor for metabolic syndrome, which may be the link between Hp-I and EAC. Although further studies are necessary to establish a pathophysiologic risk between Hp-I and the GERD−BE−EAC sequence, the theory of Hp protection against GERD seems outdated.

show abstract

Helicobacter pylori Infection and Gastric Dysbiosis: Can Probiotics Administration Be Useful to Treat This Condition?

Cited by 30 publications

References 66 publications

Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

Selected commensal bacteria change profiles of Helicobacter pylori‐induced T cells via dendritic cell modulation

Proton-Pump Inhibitors in Adults and Pediatric Patients: Use and Abuse

A perspective on risk factors for esophageal adenocarcinoma: emphasis on Helicobacter pylori infection

Contact Info

Product

Resources

About