Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1143522 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We performed RNA-seq from 6 days post fertilization hnf4a-/- and hnf4a+/+ zebrafish larval digestive tracts raised in the absence (Germ Free, GF) or presence (Conventionalized, CV) of microbiota. We found that zebrafish hnf4a activates almost half of the microbiota-suppressed genes, indicating that the microbiota supress Hnf4a trans-activity. We also provide evidence suggesting that microbial suppression of Hnf4a may contribute to IBD pathogenesis.
2017-03-27 | GSE90446 | GEO
Project description:Clostridioides difficile is one of the most common nosocomial pathogens and a global public health threat. Upon colonization of the gastrointestinal tract, C. difficile is exposed to a rapidly changing polymicrobial environment and a dynamic metabolic milieu. Despite the link between the gut microbiota and susceptibility to C. difficile, the impact of synergistic interactions between the microbiota and pathogens on the outcome of infection is largely unknown. Here, we show that microbial cooperation between C. difficile and Enterococcus has a profound impact on the growth, metabolism, and pathogenesis of C. difficile.. Through a process of nutrient restriction and metabolite cross-feeding, E. faecalis shapes the metabolic environment in the gut to enhance C. difficile fitness and increase toxin production. These findings demonstrate that members of the microbiota, such as Enterococcus, have a previously unappreciated impact on C. difficile behavior and virulence.
2022-09-17 | GSE165751 | GEO
Project description:The aquatic environment is an important site for perfluorooctanoic acid (PFOA) deposit and induced a high risk for aquatic organisms. Nevertheless, the current toxicity assessment was rarely reported the heart effect of PFOA. The exact mode of action and its resulting heterogeneity toxicological effects in aquatic organisms also remain largely unknown. In this study, the heart effects were investigated with a series of assays. The scRNA-seq showed nine cells populations were significantly altered with PFOA exposure. Heart was the mostly influenced cells and the function of cardiac muscle contraction, gas transport and oxygen binding was significantly changed. Moreover, the hatching gland cells, macrophages and lens cells were also significantly influenced with the altered function of apoptosis, endocrine and nervous and immune system. In addition, a significantly decreased swimming behavior and heart morphogenesis were verified.
2022-08-01 | GSE176853 | GEO
Project description:Dietary tannins alter growth, development, behavior, and the gut microbiome of larval amphibians
| PRJNA926636 | ENA
Project description:Purpose: The goals of this study were to evaluate the effects of acid suppression on the brain transcriptomer in a murine model of stress. In addition, the effects of the proton pump inhibitor (PPI), esomeprazole, on the brain transcriptome were evaluted in the presence or absence of stress. Methods: Male C57BL/6 mice were subjected to three days of stress by hypothermic immobilization or control environment for three hours daily and either esomeprazole 2 mg/kg or saline by intraperitoneal injection daily. Standard RNA-seq methods were employed to assess mRNA expression in the hippocampus and frontal cortex. Results: There was no effect of stress or esomeprazole on the frontal cortex transcriptome. Stress had no impact on the hippocampus transcriptome, but the addition of esomeprazole induced differential expression of 124 genes, many of which are involved in cognitive and behavior pathways. Conclusions: Further studies are needed to evaluate the associations between microbiota, host gene expression, the abundance of CNS neurocognitive modulators, and their impact on cognition and behavior.
2018-10-10 | GSE120997 | GEO
Project description:Environmental influences such as infections and dietary changes strongly affect a host’s microbiota. In the steady state, however, host genetics may influence the microbiota composition, as suggested by the greater similarity between the microbiomes of identical twin pairs compared to non-identical twins. Understanding the role of polymorphic mechanisms in regulating the commensal communities is complicated by the variability of human genomes and microbiomes, and by microbial sensitivity to the environment. Animal studies allow genetic modifications, but are also sensitive to influences known as ‘cage’ or ‘legacy’ effects. Here, we analyzed ex-germ-free mice of various genetic backgrounds, including immunodeficient and Major Histocompatibility Complex (MHC)-congenic strains repopulated with identical input microbiota. We found that the host’s genetic polymorphic mechanisms did indeed affect the gut microbiome and that both innate (e.g. anti-microbial peptides, complement, pentraxins and enzymes affecting microbial survival), as well as adaptive (both MHC-dependent and MHC-independent) pathways influenced the microbiota. These polymorphic mechanisms regulated only a limited number of microbial lineages (independently of their abundance). In addition, our comparative analyses suggested that some microbes might benefit from the specific immune responses that they elicit.
2019-08-29 | GSE136572 | GEO
Project description:Mosquitoes of the genus Aedes are primary vectors of arboviruses such as dengue, Zika, and chikungunya1. Their ability to transmit pathogens is intrinsically linked to their hematophagous behavior, which presents metabolic challenges, particularly during blood digestion2,3. One major challenge is the oxidative stress generated by heme, the prosthetic group of hemoglobin, which catalyzes the formation of reactive oxygen species (ROS)4. Excess heme can lead to cellular damage through lipid peroxidation and protein oxidation, necessitating specialized detoxification mechanisms in mosquitoes5,6.7. During blood digestion, heme concentrations in the mosquito midgut can exceed 10 mM, creating a highly oxidative environment that selects for resistant microbial species8. The midgut of A. aegypti hosts a diverse microbiota that plays a vital role in digestion, nutrient acquisition, and immune regulation9,10. Among these microbial inhabitants, bacteria of the genus Serratia are of particular interest due to their dominance in this oxidative environment11. As a Gram-negative, facultatively anaerobic bacterium, S. plymuthica exhibits resistance to oxidative stress, suggesting that it may play a role in heme homeostasis and redox balance within the mosquito midgut. Genomic analyses reveal that S. plymuthica encodes robust oxidative stress-response systems, including superoxide dismutase (sodA), catalases (katA/G), and glutathione S-transferases, which neutralize ROS and mitigate heme toxicity12. While mosquitoes have evolved antioxidant mechanisms, such as catalase induction, to mitigate heme toxicity, midgut bacteria like S. plymuthica may synergistically contribute to redox homeostasis. For instance, heme-peroxidases in mosquitoes regulate bacterial populations by modulating ROS levels and mucin crosslinking, creating a low-immunity zone that supports microbiota proliferation13. Conversely, Serratia species can internalize heme or produce antioxidant molecules, indirectly protecting the mosquito from oxidative damage while enhancing their own survival12,14,15. Such interactions are critical for maintaining microbial homeostasis and influencing vector competence, as dysbiosis in the midgut microbiota alters Plasmodium and arbovirus infections. Understanding the physiological and molecular adaptations of S. plymuthica to heme-induced oxidative stress is crucial for unraveling its survival strategies and potential role in mosquito-microbiota interactions. The midgut of A. aegypti presents a highly dynamic and oxidative environment, particularly following a blood meal, where bacterial symbionts must withstand heme toxicity while maintaining their metabolic functions12,13. We hypothesize that S. plymuthica plays an active role in mitigating oxidative stress in the mosquito gut, which may impact microbial homeostasis and vector competence. In this study, we assess the growth and oxidative stress tolerance of S. plymuthica in culture media supplemented with varying concentrations of iron and heme, coupled with a comparative proteomic analysis to identify differentially expressed proteins and metabolic pathways. By highlighting stress-response proteins, such as universal stress proteins and ABC transporters, we elucidate the adaptive mechanisms that enable S. plymuthica to persist in the mosquito midgut. These findings not only expand our understanding of mosquito-microbiota interactions but also offer new perspectives on vector competence and oxidative homeostasis, with potential implications for novel vector control strategies and biotechnological applications.
2025-07-07 | PXD062643 | Pride
Project description:Neural control of visceral organ function is essential for homeostasis and health. Intestinal peristalsis is critical for digestive physiology and host defence and is often dysregulated in gastrointestinal (GI) disorders. Luminal factors, such as diet and microbiota regulate neurogenic programs of gut motility, but the underlying molecular mechanisms remain unclear. Here we show that the transcription factor Aryl hydrocarbon Receptor (AhR) functions as a biosensor in intestinal neural circuits linking their functional output to the microbial environment of the gut lumen. Using nuclear RNA sequencing of mouse enteric neurons representing distinct intestinal segments and microbiota states, we demonstrate that the intrinsic neural networks of the colon exhibit unique transcriptional profiles controlled by the combined effects of host genetic programmes and microbial colonisation. Microbiota-induced expression of AhR in neurons of the distal gastrointestinal tract enables them to respond to the luminal environment and induce expression of neuron-specific effector mechanisms. Neuron-specific deletion of Ahr or constitutive overexpression of its negative feedback regulator CYP1A1, results in reduced peristaltic activity of the colon, similar to that observed in microbiota-depleted mice. Finally, expression of Ahr in enteric neurons of antibiotic-treated mice partially restores intestinal motility. Taken together, our experiments identify AhR signalling in enteric neurons as a regulatory node that integrates the luminal environment with the physiological output of intestinal neural circuits towards gut homeostasis and health. The enteric nervous system (ENS) encompasses the intrinsic neural networks of the gastrointestinal (GI) tract, which regulate most aspects of intestinal physiology, including peristalsis. In addition to host-specific genetic programmes, microbiota and diet have emerged as critical regulators of gut tissue physiology and changes in the microbial composition of the lumen often accompany GI disorders. However the molecular mechanisms by which gut enviromental factors regulate ENS homeostasis remain unknown. In order to address this issue, we used RNA sequencing to identify genes specifically upregulated in mouse colonic neurons in response to microbial colonisation.
2019-11-13 | GSE140291 | GEO
Project description:Neural control of visceral organ function is essential for homeostasis and health. Intestinal peristalsis is critical for digestive physiology and host defence and is often dysregulated in gastrointestinal (GI) disorders. Luminal factors, such as diet and microbiota regulate neurogenic programs of gut motility, but the underlying molecular mechanisms remain unclear. Here we show that the transcription factor Aryl hydrocarbon Receptor (AhR) functions as a biosensor in intestinal neural circuits linking their functional output to the microbial environment of the gut lumen. Using nuclear RNA sequencing of mouse enteric neurons representing distinct intestinal segments and microbiota states, we demonstrate that the intrinsic neural networks of the colon exhibit unique transcriptional profiles controlled by the combined effects of host genetic programmes and microbial colonisation. Microbiota-induced expression of AhR in neurons of the distal gastrointestinal tract enables them to respond to the luminal environment and induce expression of neuron-specific effector mechanisms. Neuron-specific deletion of Ahr or constitutive overexpression of its negative feedback regulator CYP1A1, results in reduced peristaltic activity of the colon, similar to that observed in microbiota-depleted mice. Finally, expression of Ahr in enteric neurons of antibiotic-treated mice partially restores intestinal motility. Taken together, our experiments identify AhR signalling in enteric neurons as a regulatory node that integrates the luminal environment with the physiological output of intestinal neural circuits towards gut homeostasis and health. The enteric nervous system (ENS) encompasses the intrinsic neural networks of the gastrointestinal (GI) tract, which regulate most aspects of intestinal physiology, including peristalsis. In addition to host-specific genetic programmes, microbiota and diet have emerged as critical regulators of gut tissue physiology and changes in the microbial composition of the lumen often accompany GI disorders. However the molecular mechanisms by which gut enviromental factors regulate ENS homeostasis remain unknown. In order to address this issue, we used RNA sequencing to identify genes specifically upregulated in mouse colonic neurons in response to microbial colonisation.
2019-11-13 | GSE140290 | GEO