Detecting host responses to microbial stimulation using primary epithelial organoids.

The intestinal epithelium is constantly exposed to microbes residing in the lumen. Traditionally, the response to microbial interactions has been studied in cell lines derived from cancerous tissues, e.g.

Personalized B cell response to the probiotic in healthy human subjects: a randomized trial.

The specific effects of administering live probiotics in the human gut are not well characterized. To this end, we investigated the immediate effect of GG (LGG) in the jejunum of 27 healthy volunteers 2 h after ingestion using a combination of global RNA sequencing of human biopsies and bacterial DNA sequencing in a multi-visit, randomized, cross-over design (ClinicalTrials.gov number NCT03140878).

Bacterial infection increases risk of carcinogenesis by targeting mitochondria.

As up to a fifth of all cancers worldwide, have now been linked to microbial infections, it is essential to understand the carcinogenic nature of the bacterial/host interaction. This paper reviews the bacterial targeting of mediators of mitochondrial genomic fidelity and of mitochondrial apoptotic pathways, and compares the impact of the bacterial alteration of mitochondrial function to that of cancer. Bacterial virulence factors have been demonstrated to induce mutations of mitochondrial DNA (mtDNA) and to modulate DNA repair pathways of the mitochondria.

Enterococcus faecalis Infection and Reactive Oxygen Species Down-Regulates the miR-17-92 Cluster in Gastric Adenocarcinoma Cell Culture.

Chronic inflammation due to bacterial overgrowth of the stomach predisposes to the development of gastric cancer and is also associated with high levels of reactive oxygen species (ROS). In recent years increasing attention has been drawn to microRNAs (miRNAs) due to their role in the pathogenesis of many human diseases including gastric cancer. Here we studied the impact of infection by the gram-positive bacteria Enterococcus faecalis (E.

Impact of bacterial infections on aging and cancer: impairment of DNA repair and mitochondrial function of host cells.

The commensal floras that inhabit the gastrointestinal tract play critical roles in immune responses, energy metabolism, and even cancer prevention. Pathogenic and out of place commensal bacteria, can however have detrimental effects on the host, by introducing genomic instability and mitochondrial dysfunction, which are hallmarks of both aging and cancer. Helicobacter pylori and Enterococcus faecalis are bacteria of the gastrointestinal tract that have been demonstrated to affect these two hallmarks.

Helicobacter pylori infection affects mitochondrial function and DNA repair, thus, mediating genetic instability in gastric cells.

Helicobacter pylori infection is an important factor for the development of atrophic gastritis and gastric carcinogenesis. However, the mechanisms explaining the effects of H. pylori infection are not fully elucidated.

Enterococcus faecalis infection causes inflammation, intracellular oxphos-independent ROS production, and DNA damage in human gastric cancer cells.

Background: Achlorhydria caused by e.g. atrophic gastritis allows for bacterial overgrowth, which induces chronic inflammation and damage to the mucosal cells of infected individuals driving gastric malignancies and cancer.

Interferon-γ inhibits ghrelin expression and secretion via a somatostatin-mediated mechanism.

Aim: To investigate if and how the proinflammatory cytokine interferon γ (IFNγ) affects ghrelin expression in mice.

Methods: The plasma concentration of ghrelin, and gastric ghrelin and somatostatin expression, were examined in wild-type mice and mice infected with Helicobacter pylori (H. pylori).