Characterising Commensal and Pathogenic Staphylococcal Interactions with Neonatal and Adult Blood
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PROVIDER: PRJEB85410 | ENA |
REPOSITORIES: ENA
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Project description:Peripheral blood samples (0.45 ml) were collected from 8 preterm infants (30–32 weeks gestational age [GA]), 8 term infants (37–41 weeks) GA, and 8 adults (18–25 years). Samples were challenged ex vivo with a defined dose of approximately 1x10^7 colony-forming units (CFU) of either Staphylococcus epidermidis WT 1457 or Staphylococcus aureus ATCC 29523 for 90 minutes. An additional aliquot (0.1 ml) from each participant’s blood was retained as an unstimulated baseline control. Following the bacterial challenge, a previously optimized RNA extraction protocol was employed to isolate total RNA from leukocytes and bacteria in all samples (n = 72). Ribosomal RNA was depleted from the purified RNA, which was subsequently sequenced using 150 bp paired-end reads on a NovaSeq 6000 platform (Illumina). Sequencing reads were aligned to host and bacterial reference genomes in silico, and bioinformatic analyses were performed to investigate host- and pathogen-specific transcriptional changes associated with early infection in this sepsis model.
2025-03-02 | E-MTAB-14798 | biostudies-arrayexpress
Project description:Early life microbe-immune interactions at barrier surfaces have lasting impacts on the trajectory towards health versus disease. Monocytes, macrophages and dendritic cells are primary sentinels in barrier tissues, yet the salient contributions of commensal-myeloid crosstalk during tissue development remain poorly understood. Here, we identify that commensal microbes facilitate accumulation of a population of monocytes in neonatal skin. Transient postnatal depletion of these monocytes resulted in heightened IL-17A production by skin T cells, which was particularly sustained among CD4+ T cells into adulthood and sufficient to exacerbate inflammatory skin pathologies. Neonatal skin monocytes were enriched in expression of negative regulators of the IL-1 pathway. Functional in vivo experiments confirmed a key role for excessive IL-1R1 signaling in T cells as contributing to the dysregulated type 17 response in neonatal monocyte-depleted mice. Thus, a commensal-driven wave of monocytes into neonatal skin critically facilitates immune homeostasis in this prominent barrier tissue.
2026-01-20 | GSE294110 | GEO
Project description:Early life microbe-immune interactions at barrier surfaces have lasting impacts on the trajectory towards health versus disease. Monocytes, macrophages and dendritic cells are primary sentinels in barrier tissues, yet the salient contributions of commensal-myeloid crosstalk during tissue development remain poorly understood. Here, we identify that commensal microbes facilitate accumulation of a population of monocytes in neonatal skin. Transient postnatal depletion of these monocytes resulted in heightened IL-17A production by skin T cells, which was particularly sustained among CD4+ T cells into adulthood and sufficient to exacerbate inflammatory skin pathologies. Neonatal skin monocytes were enriched in expression of negative regulators of IL-1 pathway. Functional in vivo experiments confirmed a key role for excessive IL-1R1 signaling in T cells as contributing to the dysregulated type 17 response in neonatal monocyte-depleted mice. Thus, a commensal-driven wave of monocytes into neonatal skin critically facilitates long-term immune homeostasis in this prominent barrier tissue.
2025-03-01 | GSE244177 | GEO
Project description:Transcriptome profiling of E. coli MG1655, E. coli EDL933, E. coli ECOR26, and E. coli Nissle 1917 grown on mouse cecal mucus as carbon source The carbon sources that support growth of pathogenic E. coli O157:H7 in the mammalian intestine have not previously been investigated. In vivo, pathogenic E. coli EDL933 primarily grows as dispersed single cells within the mucus layer that overlies the mouse cecal epithelium. We therefore compared the pathogen and commensal E. coli MG1655 for their mode of metabolism in vitro on a mixture of the sugars known to be present in cecal mucus and found that the two strains used the thirteen sugars in a similar order and co-metabolized as many as nine sugars at a time. We conducted a systematic mutational analysis of E. coli EDL933 and E. coli MG1655 with lesions in the pathways used for catabolism of thirteen mucus-derived sugars and five other compounds for which the corresponding gene system was induced in the transcriptome of cells grown on cecal mucus. Each of 18 catabolic mutants in both genetic backgrounds was fed to streptomycin-treated mice together with the respective wildtype parent strain and their colonization was monitored in fecal plate counts. None of the mutations corresponding to the five compounds not found in mucosal polysaccharides resulted in colonization defects. Based on the mutations that caused colonization defects, we determined that both E. coli EDL933 and E. coli MG1655 used arabinose, fucose, and N-acetylglucosamine in the intestine. In addition, E. coli EDL933 used galactose, hexuronates, mannose and ribose, whereas E. coli MG1655 used gluconate and N-acetylneuraminic acid. The colonization defects of six catabolic lesions were found to be additive in E. coli EDL933, but not E. coli MG1655. The data indicate that pathogenic E. coli EDL933 uses sugars that are not used by commensal E. coli MG1655 to colonize the mouse intestine. The results suggest a strategy whereby invading pathogens gain advantage by simultaneously consuming several sugars that may be available because they are not consumed by the commensal intestinal microbiota. Keywords: growth condition: carbon source was mouse cecal mucus E. coli strains were grown on MOPS minimal medium containing 10 mg/ml of mucus or 0.2% glucose in 10 ml standing culture in testtubes and harvested at OD600 = 0.4.
2008-04-25 | E-GEOD-11254 | biostudies-arrayexpress
Project description:Transcriptome profiling of E. coli MG1655, E. coli EDL933, E. coli ECOR26, and E. coli Nissle 1917 grown on mouse cecal mucus as carbon source The carbon sources that support growth of pathogenic E. coli O157:H7 in the mammalian intestine have not previously been investigated. In vivo, pathogenic E. coli EDL933 primarily grows as dispersed single cells within the mucus layer that overlies the mouse cecal epithelium. We therefore compared the pathogen and commensal E. coli MG1655 for their mode of metabolism in vitro on a mixture of the sugars known to be present in cecal mucus and found that the two strains used the thirteen sugars in a similar order and co-metabolized as many as nine sugars at a time. We conducted a systematic mutational analysis of E. coli EDL933 and E. coli MG1655 with lesions in the pathways used for catabolism of thirteen mucus-derived sugars and five other compounds for which the corresponding gene system was induced in the transcriptome of cells grown on cecal mucus. Each of 18 catabolic mutants in both genetic backgrounds was fed to streptomycin-treated mice together with the respective wildtype parent strain and their colonization was monitored in fecal plate counts. None of the mutations corresponding to the five compounds not found in mucosal polysaccharides resulted in colonization defects. Based on the mutations that caused colonization defects, we determined that both E. coli EDL933 and E. coli MG1655 used arabinose, fucose, and N-acetylglucosamine in the intestine. In addition, E. coli EDL933 used galactose, hexuronates, mannose and ribose, whereas E. coli MG1655 used gluconate and N-acetylneuraminic acid. The colonization defects of six catabolic lesions were found to be additive in E. coli EDL933, but not E. coli MG1655. The data indicate that pathogenic E. coli EDL933 uses sugars that are not used by commensal E. coli MG1655 to colonize the mouse intestine. The results suggest a strategy whereby invading pathogens gain advantage by simultaneously consuming several sugars that may be available because they are not consumed by the commensal intestinal microbiota. Keywords: growth condition: carbon source was mouse cecal mucus
2008-04-25 | GSE11254 | GEO
Project description:Early life establishment of tolerance to commensal bacteria at barrier surfaces carries enduring implications for immune health but remains poorly understood. Here we show that this process is controlled by microbial interaction with a specialized subset of antigen presenting cells. More particularly, we identify CD301b+ type 2 conventional dendritic cells (DC) as a subset in neonatal skin specifically capable of uptake, presentation and generation of regulatory T cells (Tregs) to commensal antigens. In early life, CD301b+ DC2 are enriched for programs of phagocytosis and maturation, while also expressing tolerogenic markers. In both human and murine skin, these signatures were reinforced by microbial uptake. In contrast to their adult counterparts or other early life DC subsets, neonatal CD301b+ DC2 highly expressed the retinoic acid-producing enzyme, RALDH2, deletion of which limited commensal-specific Tregs. Thus, synergistic interactions between bacteria and a specialized DC subset critically support early life tolerance at the cutaneous interface.
2023-01-01 | GSE206892 | 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: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:Commensal myeloid crosstalk in neonatal skin regulates cutaneous type 17 inflammation
| PRJNA1248404 | ENA
Project description:Aberrant CD4+ T cell reactivity against intestinal microbes is considered to drive mucosal inflammation in inflammatory bowel diseases. The disease-relevant microbial species and the corresponding microbe-specific pathogenic T cell phenotypes remain unknown. Here, we identify common gut commensal and food-derived yeasts, as direct activators of aberrant CD4+ T cell reactions in patients with Crohn´s disease (CD). Yeast-responsive CD4+ T cells in CD display a cytotoxic Th1 phenotype and selective clonal expansion of cells highly cross-reactive to several commensal, as well as food-derived, fungal species. This indicates cross-reactive T cell selection by repeated encounter with conserved fungal antigens in the context of chronic intestinal disease. Our results highlight a role of fungi in driving immunopathology in patients with CD and suggest that both, gut-resident fungal commensals, and daily dietary intake of yeasts, may contribute to chronic activation of pathogenic CD4+ T cell responses involved in disease pathophysiology.
2023-08-15 | GSE227638 | GEO