Association of multiresistant enteric pathogens between human and animal interface.
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB23049 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Disease outbreaks due to the consumption of legume seedlings contaminated with human enteric bacterial pathogens like Escherichia coli O157:H7 and Salmonella enterica are reported every year. We found surface and internal colonization of Medicago truncatula by Salmonella enterica and Escherichia coli O157:H7 even with inoculum levels as low as two bacteria per plant. Expression analyses using microarray revealed that some Medicago truncatula genes were regulated in a similar manner in response to both of these enteric pathogens. Medicago truncatula roots were inoculated with low inoculum levels of two enteric bacteria per plant (E. coli O157:H7 and Salmonella). 10 days post inoculated plants were used for RNA extraction and hybridization on Affymetrix microarrays.
2013-12-18 | E-GEOD-53406 | biostudies-arrayexpress
Project description:Examination of intestinal colonization of enteric pathogen Salmonella typhimurium
2015-08-14 | MSV000079240 | MassIVE
Project description:Disease outbreaks due to the consumption of legume seedlings contaminated with human enteric bacterial pathogens like Escherichia coli O157:H7 and Salmonella enterica are reported every year. We found surface and internal colonization of Medicago truncatula by Salmonella enterica and Escherichia coli O157:H7 even with inoculum levels as low as two bacteria per plant. Expression analyses using microarray revealed that some Medicago truncatula genes were regulated in a similar manner in response to both of these enteric pathogens.
2013-12-18 | GSE53406 | GEO
Project description:The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss and dysmotility during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via b2-adrenergic receptors (b2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemic production of interleukin (IL)-4 and -13 by eosinophils, which induced arginase-expressing MMs that prevented neuronal loss from an unrelated infection located in a different intestinal region. Collectively, these data suggest that distinct enteric pathogens trigger a state of disease- or tissue tolerance that preserves ENS number and functionality.
2021-08-17 | GSE182294 | GEO
Project description:BACKGROUND Enteric glia contribute to the pathophysiology of various intestinal immune-driven diseases, such as postoperative ileus (POI), a motility disorder and common complication after abdominal surgery. Enteric gliosis of the intestinal muscularis externa (ME) has been identified as part of POI development. However, the glia-restricted responses and activation mechanisms are poorly understood. The sympathetic nervous system becomes rapidly activated by abdominal surgery. It modulates intestinal immunity, innervates all intestinal layers, and directly interfaces with enteric glia. We hypothesized that sympathetic innervation controls enteric glia reactivity in response to surgical trauma. METHODS Sox10iCreERT2/Rpl22HA/+ mice were subjected to a mouse model of laparotomy or intestinal manipulation to induce POI. Histological, protein, and transcriptomic analyses were performed to analyze glia-specific responses. Interactions between the sympathetic nervous system and enteric glia were studied in mice chemically depleted of TH+ sympathetic neurons and glial-restricted Sox10iCreERT2/JellyOPfl/+/Rpl22HA/+ mice, allowing optogenetic stimulation of β-adrenergic downstream signaling and glial-specific transcriptome analyses. A laparotomy model was used to study the effect of sympathetic signaling on enteric glia in the absence of intestinal manipulation. Mechanistic studies included adrenergic receptor expression profiling in vivo and in vitro and adrenergic agonism treatments of primary enteric glial cell cultures to elucidate the role of sympathetic signaling in acute enteric gliosis and POI. RESULTS With ~4000 differentially expressed genes, the most substantial enteric glia response occurs early after intestinal manipulation. During POI, enteric glia switch into a reactive state and continuously shape their microenvironment by releasing inflammatory and migratory factors. Sympathetic denervation reduced the inflammatory response of enteric glia in the early postoperative phase. Optogenetic and pharmacological stimulation of β-adrenergic downstream signaling triggered enteric glia reactivity. Finally, distinct adrenergic agonists revealed β-1/2 adrenoceptors as the molecular targets of sympathetic–driven enteric glial reactivity. CONCLUSIONS Enteric glia act as early responders during post-traumatic intestinal injury and inflammation. Intact sympathetic innervation and active β-adrenergic receptor signaling in enteric glia is a trigger of the immediate glial postoperative inflammatory response. With immune-activating cues originating from the sympathetic nervous system as early as the initial surgical incision, adrenergic signaling in enteric glia presents a promising target for preventing POI development.
2023-11-15 | GSE198889 | GEO
Project description:Enteric glia are the predominant cell type in the enteric nervous system yet their identities and roles in gastrointestinal function are not well classified. Using our optimized single nucleus RNA-sequencing method, we identified distinct molecular classes of enteric glia and defined their morphological and spatial diversity. Our findings revealed a functionally specialized biosensor subtype of enteric glia that we call “hub cells.” Deletion of the mechanosensory ion channel PIEZO2 from adult enteric glial hub cells, but not other subtypes of enteric glia, led to defects in intestinal motility and gastric emptying in mice. These results provide insight into the multifaceted functions of different enteric glial cell subtypes in gut health and emphasize that therapies targeting enteric glia could advance the treatment of gastrointestinal diseases.
2023-09-08 | GSE232703 | GEO
Project description:Endocannabinoids inhibit induction of virulence in enteric pathogens
| PRJEB29880 | ENA
Project description:The serotonin neurotransmitter modulates virulence of enteric pathogens
| PRJNA604962 | ENA
Project description:Enteric Glia treated with exATP
2020-11-15 | GSE134941 | GEO
Project description:Identification of cellular functions and signalling pathways of intestinal epithelial cells modulated by enteric glial cells Keywords: Transcriptome regulation Two-condition experiment (intestinal epithelial cells cultured in absence or in presence of enteric glial cells) with 3 time points (t=0, 8 and 24h). 4 Biological replicates/condition. Every replicate was hybridized against a reference pool composed by a mix of the 4 replicates of t=0 condition in equal quantity.
2010-05-16 | E-GEOD-17027 | biostudies-arrayexpress