Bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB17409 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR527087_1.fastq.gz | Fastqsanger.gz | |||
| DRR527087_2.fastq.gz | Fastqsanger.gz | |||
| DRR527088_1.fastq.gz | Fastqsanger.gz | |||
| DRR527088_2.fastq.gz | Fastqsanger.gz | |||
| DRR527089_1.fastq.gz | Fastqsanger.gz |
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Project description:An essential function of the liver is the formation of bile. This aqueous solution is critical for fat absorption and is transported to the duodenum via the common bile duct. Despite extensive studies of bile salts, other components of bile are less well-charted. Here, we characterized the murine bile metabolome and investigated how the microbiota and enteric infection influence bile composition. We discovered that the bile metabolome is not only substantially more complex than appreciated but is dynamic and responsive to the microbiota and enteric infection. Hepatic transcriptomics identified enteric infection-triggered pathways that likely underlie bile remodeling. Enteric infections stimulated elevation of four dicarboxylates in bile that modulated intestinal gut epithelial and microbiota composition, inflammasome activation, and host defense. Our data suggest that enteric infection-associated signals are relayed between the intestine and liver and induce transcriptional programs that shape the bile metabolome, modifying bile’s immunomodulatory and host defense functions.
2023-05-02 | GSE227180 | GEO
Project description:Early life gut microbiota plays a critical role in gut development, maturation of the immune response and protection against enteric pathogens such as Salmonella. In this study, we investigated how different gut microbiota compositions influence the host transcriptomic signatures and susceptibility to Salmonella infection in chicks.
2025-11-30 | E-MTAB-16061 | biostudies-arrayexpress
Project description:Characterization of the human microbiota is providing new insightsinto the complexity of host–parasite–bacterium relationships. Amoebiasis (an intestinal infection affecting a large proportion of the population in many countries worldwide) is caused by the amoebic parasite Entamoeba histolytica. During amoebiasis, the parasite encounters several types of stress as a result of the host’s response to infection. Given that E. histolytica phagocytises bacteria in the intestinal lumen, we hypothesized that enteric bacteria can influence the course of an amoebic infection. Hence, we used live Escherichia coli O55 as a pertinent model of the bacterial community’s contribution to amoebic responses during host- induced stress. By measuring amoebic survival, we found that live E. coli protected E. histolytica against oxidative stress (OS) but not against nitrosative stress. E. coli– associated protection is correlated with massive transcriptionalchanges in amoebic genes acquired through lateral transfer from the bacterial kingdom, including genes coding for proteinscontaining leucine-rich repeat (LRR) motifs. The transcriptome profile triggered by OS and E. coli was also observed with other enteric bacteria, including pathogens and non-pathogens. In contrast, exposure to a probiotic resulted in a different transcriptome profile. The present study shows that OS and live bacteria together modulate 84 of E. histolytica’s 137 LRR protein genes. The LRR proteins are involvedin protein-ligand and protein-protein interactions – especially in proteins that interact with bacteria as part of the innate immune response in mammals and plants, such as Toll-like receptors. The structural and functional homology of LRRs and TLRs identified here suggest that despite its old age in evolutionary terms, the protozoan E. histolytica displays key characteristics of higher eukaryotes’ innate immune systems. We conclude that components of innate immunity existed in the common ancestor of plants and animals
2018-06-08 | GSE104434 | GEO
Project description:We used the ileal loop model to assess the effects of enteric bacteria organisms on host gene expression in intestinal tissue independent of and following early SIV infection. SIV infection in the gut causes rapid and severe immune dysfunction and damage to the intestinal structure, this may alter the intimate interaction with lumenal organisms. This study was performed to determine whether early SIV infection, prior to the depletion of CD4+ T cells, can alter interaction of the host with pathogenic Salmonella serovar Typhimurium (ST) or commensal Lactobacillus plantarum (LP), and to further understand the earliest changes to the intestinal mucosa following SIV infection. We used microarray analysis to detail the global program of gene expression underlying changes in the ileum following early SIV infection, and if these changes in any way alter the host interaction/ response to pathogenic and commensal enteric bacteria.
2014-12-19 | GSE52589 | GEO
Project description:Microbial density and diversity increase in distal intestinal segments, affecting tissue physiology, metabolism, and function of both the immune and nervous systems. We characterized the influence of the microbiota on murine intrinsic enteric-associated neurons (iEAN). We found that iEAN are functionally adapted to the intestinal segment they occupy, with a stronger microbiota influence on ileal and colonic neurons. Chemogenetic characterization of microbiota-influenced iEAN identified a subset of viscerofugal CART+ neurons, enriched in the ileum and colon, able to modulate feeding and glucose metabolism. Retro- and anterograde tracing revealed that CART+ viscerofugal neurons send axons to the prevertebral ganglia and are poly-synaptically connected to the liver and pancreas. Microbiota depletion led to NLRP6 and Caspase 11-dependent loss of CART+ neurons, and impaired liver-mediated gluconeogenesis. Our results demonstrate a region-specific adaptation of enteric neurons and indicate that iEAN subsets are capable of regulating blood glucose levels independently from the central nervous system.
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Project description:Complex gut microbiota increases chicken resistance to enteric diseases. However, the principles of this phenomenon are not understood in detail. One of the possibilities how to decipher the role of gut microbiota in chicken resistance to enteric pathogens is to gradually characterise gene expression of individual gut microbiota members when colonising chicken caecum. To reach this aim, newly hatched chicks were inoculated with bacterial species with known whole genomic sequence. Total protein purified from the chicken caecum was analysed by mass spectrometry and obtained spectra were searched against strain-specific protein databases generated from known genomic sequences.
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Project description:We used the ileal loop model to assess the effects of enteric bacteria organisms on host gene expression in intestinal tissue independent of and following early SIV infection. SIV infection in the gut causes rapid and severe immune dysfunction and damage to the intestinal structure, this may alter the intimate interaction with lumenal organisms. This study was performed to determine whether early SIV infection, prior to the depletion of CD4+ T cells, can alter interaction of the host with pathogenic Salmonella serovar Typhimurium (ST) or commensal Lactobacillus plantarum (LP), and to further understand the earliest changes to the intestinal mucosa following SIV infection. We used microarray analysis to detail the global program of gene expression underlying changes in the ileum following early SIV infection, and if these changes in any way alter the host interaction/ response to pathogenic and commensal enteric bacteria. A subset of animals were infected with SIVmac251 for 2.5 days, following which they underwent a loop surgery where the ileum was sectioned off with surgical ties and bacteria (ST or LP) or their respective media controls (LB or MRS) were injected intralumenally. Following 5 hours of incubation the loops were excised and frozen. Tissue sections were cut and RNA extracted for gene expression analysis. Rhesus Macaques infected with SIVmac251 for 2.5 days compared to uninfected controls. Comparisons are of ileum loop sections injected with Salmonella serovar Typhimurium, Lactobacillus Plantarum or respective media controls LB or MRS.
2014-12-19 | E-GEOD-52589 | biostudies-arrayexpress
Project description:The mosquito Anopheles gambiae uses its innate immune system to control bacterial and Plasmodium infection of its midgut tissue. The activation of potent IMD pathway-mediated anti-Plasmodium falciparum defenses is dependent on the presence of the midgut microbiota, which activate this defense system upon parasite infection through a peptidoglycan recognition protein, PGRPLC. We employed transcriptomic and reverse genetic analyses to compare the P. falciparum infection-responsive transcriptomes of septic and aseptic mosquitoes and to determine whether bacteria-independent anti-Plasmodium defenses exist. To examine the impact of P. falciparum infection on the mosquito midgut and carcass transcriptomes in the presence or absence of midgut bacteria, we used A. gambiae whole genome microarrays to compare the mRNA abundance of P. falciparum-infected and -naïve mosquitoes of antibiotic- and non-antibiotic treated cohorts. P. falciparum infection induced changes in the abundance of as many as 2,183 and 2,429 transcripts in whole mosquitoes belonging to a variety of functional groups in aseptic and septic mosquitoes. Ultimately, we were interested in identifying the genes involved in bacteria-independent anti-Plasmodium responses, and therefore we focused on transcripts displaying increased abundance in the parasite-infected aseptic midguts, placing a particular emphasis on those with predicted immune functions. Because of the central role of serine protease cascades in regulating insect immune defenses, we focused the remainder of our analysis on a clip-domain serine protease C2 (CLIPC2, AGAP004317) and a serine protease inhibitor 7 (SRPN7, AGAP007693) that were specifically upregulated in the parasite-infected, aseptic mosquito midgut. We showed that SRPN7 negatively and CLIPC2 positively regulate the anti-Plasmodium defense, independently of the midgut-associated bacteria. Co-silencing assays suggested that these two genes may function together in a signaling cascade. Neither gene was regulated, nor modulated, by infection with the rodent malaria parasite Plasmodium berghei, suggesting that SRPN7 and CLIPC2 are components of a defense system with preferential activity towards P. falciparum. Further analysis using RNA interference determined that these genes do not regulate the anti-Plasmodium defense mediated by the IMD pathway, and both factors act as agonists of the endogenous midgut microbiota, further demonstrating the lack of functional relatedness between these genes and the bacteria-dependent activation of the IMD pathway. This is the first study confirming the existence of a bacteria-independent, anti-P. falciparum defense. Aseptic and septic midguts and carcasses from P. falciparum-infected A. gambiae vs aseptic and septic midguts and carcasses from uninfected, blood-fed A. gambiae. 3 biological replicates and 1 pseudo-replicate per each array.
2013-08-10 | E-GEOD-49690 | biostudies-arrayexpress
Project description:Enteric–associated neurons (EAN) are closely associated with immune cells and continuously monitor and modulate homeostatic intestinal functions, including motility. Bidirectional interactions between immune and neuronal cells are altered during disease processes such as neurodegeneration or irritable bowel syndrome. We investigated how infection-induced inflammation affects intrinsic EAN (iEAN) and the role of intestinal muscularis macrophages (MM) in this process. Using murine models of enteric infections, we observed long-term gastrointestinal symptoms including reduced motility and loss of excitatory iEAN, which was mediated by an NLRP6 and caspase 11 mechanism, depended on infection history, and could be reversed by microbiota manipulation. MM responded to luminal infection by upregulating a neuroprotective program dependent on β2-adrenergic receptor (β2-AR) signaling, and mediated neuronal protection via an arginase 1-polyamine axis. Our results identify a mechanism of neuronal cell death post–infection and point to a role for tissue–resident MM in limiting neuronal damage.
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Project description:The role of the microbiota in facilitating infections is increasingly recognized, though the underlying mechanisms remain under investigation. In this study, we demonstrate that the gut microbiome, particularly Lactiplantibacillus plantarum, promotes enteric infection in Drosophila melanogaster by reshaping host physiology and immune responses. Upon gut colonization, L. plantarum enhances fatty acid (FA) production in the gut. Reducing FA synthesis improves host survival, and pathogen mutants deficient in FA utilization exhibit reduced virulence. FAs support pathogen growth, increase virulence, and enhance resistance to antimicrobial effectors, ultimately facilitating pathogen persistence in the gut. Persisting pathogens consequently overstimulate the immune system, leading to excessive production of antimicrobial peptides (AMPs). Flies lacking AMPs, particularly Metchnikowin and Attacin D mutants, show better survival during infection, implicating AMPs in immunopathology. Our findings identify a mechanism whereby microbiota-induced release of host FAs stimulates pathogen virulence and persistence, ultimately driving AMP-mediated immunopathology.
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