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E-cigarettes compromise the gut barrier, trigger inflammation

ABSTRACT: E-cigarettes compromise the gut barrier, trigger inflammation

PROVIDER: PRJNA678641 | ENA |

REPOSITORIES: ENA

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E-cigarettes compromise the gut barrier, trigger inflammation

Project description:Despite the rising popularity of e-cigarette and vaping devices, their safety continues to be questioned. Using established murine models of acute and chronic e-cigarette aerosol inhalation, murine colon transcriptomics and organoid co-culture models, here we assessed the effects of e-cigarette use on the gut barrier. Histologic and transcriptome analyses revealed that chronic, but not acute, nicotine-free e-cigarette use was associated with inflammation and reduced expression of tight junction markers, including occludin. Exposure of murine and human enteroid-derived monolayers (EDMs) to nicotine-free e-cigarette aerosols alone or in co-culture with invasive E. coli, recapitulated the key findings observed in vivo, i.e., barrier-disruption, downregulation of occludin, inflammation, and an accentuated risk of and response to bacterial infection. These data highlight an unexpected harmful effect of ecigarette use on the gut barrier and pinpoint non-nicotine chemical components as the source of harm. Considering the importance of an intact gut barrier for host fitness, and the impact of gut mucosal inflammation on a multitude of chronic diseases, these findings are broadly relevant to medicine and public health.

2020-11-17 | GSE161521 | GEO

Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.

2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress

E-cigarettes compromise the gut barrier and trigger inflammation.

Project description: Not available

| S-EPMC7841355 | biostudies-literature

Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

Project description:Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

| PRJEB12103 | ENA

Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

Project description:Opioid-induced gut microbial disruption leads to gut barrier compromise and sustained systemic inflammation.

| PRJEB12086 | ENA

Contributions of microbiome and mechanical deformation to intestinal bacterial overgrowth and inflammation in a human gut-on-a-chip.

Project description:A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1Î², and TNF-Î±) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models. 6 samples, 2 biological replicates for each 3 conditions.

2015-12-16 | E-GEOD-65790 | biostudies-arrayexpress

Revisiting the putative role of heme as a trigger of inflammation

Project description:Revisiting the putative role of heme as a trigger of inflammation

2020-07-10 | GSE101793 | GEO

Opioid-induced gut microbial disruption and bile dysregulation leads to gut barrier compromise and sustained systemic inflammation.

Project description: Not available

| S-EPMC4996771 | biostudies-literature

Contributions of microbiome and mechanical deformation to intestinal bacterial overgrowth and inflammation in a human gut-on-a-chip

Project description:A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1β, and TNF-α) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models.

2015-12-16 | GSE65790 | GEO

C-section delivery related high sensitivity to inflammation in mice is unchained by gut barrier-microbiota imbalances in the early life

Project description:The main goal of this study is to decipher the role of CSD in the early-life gut microbiota-barrier alterations and its links with later-life risks of intestinal inflammation

2022-10-02 | GSE214311 | GEO

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