Bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA492917 | ENA |
REPOSITORIES: ENA
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Project description:Competition for limited iron resources is a key driver of microbial community structure in many regions of the surface ocean. The bacterial siderophores ferrioxamine and amphibactin have been identified in marine surface waters, suggesting that they may represent an important bacterial strategy for obtaining iron from a scarcely populated pool. We screened several strains of marine Vibrio for the presence of putative amphibactin biosynthesis gene homologues and amphibactin production. Whole cell proteomics, siderophore isolation, and isotopically labeled iron uptake experiments were performed. Here, we show that an amphibactin-producing marine bacterium, Vibrio cyclitrophicus str. 1F-53, harbors an independently regulated uptake pathway for ferrioxamines. Proteomic analyses identified upregulation of the amphibactin NRPS system and a putative amphibactin siderophore transporter in response to low iron concentrations. In addition, multiple other transporters were upregulated, however when desferrioxamine was present, amphibactin production decreased and the ferrioxamine receptor increased in abundance. Such cheating phenotypes, which appear widespread among marine amphibactin producers, highlight the strategies that contribute to the fitness of marine bacteria in the face of iron stress. These results demonstrate siderophore producer and cheater phenotypes and highlight the cellular restructuring which is involved due to competition for iron, that shapes the community structure of marine ecosystems.
2021-04-19 | PXD011427 | Pride
Project description:Protection against pathogens is a major function of the gut microbiota. Although bacterial natural products have emerged as crucial components of host-microbiota interactions, their exact role in microbiota-mediated protection is largely unexplored. We addressed this knowledge gap with the nematodeCaenorhabditis elegansand its microbiota isolatePseudomonas fluorescensMYb115 that is known to protect againstBacillus thuringiensis (Bt) infection. We find that MYb115-mediated protection depends on sphingolipids that are derived from an iterative type I polyketide synthase (PKS), thereby describing a noncanonical pathway of bacterial sphingolipid production. We provide evidence that MYb115-derived sphingolipids affectC. eleganstolerance to Bt infection by altering host sphingolipid metabolism. This work establishes sphingolipids as structural outputs of bacterial PKS and highlights the role of microbiota-derived sphingolipids in host protection against pathogens.
2023-10-14 | GSE245296 | GEO
Project description:A special immune system exists at distinct respiratory epithelium to combat invasion by Pseudomonas aeruginosa (PAO1). This study aimes to determine if interleukin-17C (IL-17C) is correlated with acute PAO1 infection in human nasal epithelium and to prove the role of IL-17C on iron sequestration during PAO1 infection. IL-17C has antipseudomonal effect by lowering iron sequestration and reducing siderophore activity. IL-17C could be efficient mediator to control PAO1 infection in human nasal epithelium.
2018-01-12 | GSE109118 | GEO
Project description:Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Using gnotobiotic mouse models, we provide a systematic analysis of the role of microbiota in the induction of cytokine responses in the normal intestine. Colonization by a whole mouse microbiota orchestrated a broad spectrum of pro-inflammatory (Th1, Th17) and regulatory T cell responses. Unexpectedly, most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal cytokine responses. A potent cytokine-inducing function was however associated with non-culturable host-specific species, the prototype of which was the Clostridia-related Segmented Filamentous Bacterium, and this bacterial species recapitulated the coordinated maturation of T cell responses induced by the whole mouse microbiota. Our study demonstrates the non-redundant role of microbiota members in the regulation of gut immune homeostasis. Germfree (GF) female 8-9-week-old mice were gavaged twice at a 24-hr interval with 0.5 mL of fresh anaerobic cultures of fecal homogenate from SFB mono-associated mice, fresh feces from Cv mice (Cvd) or from a healthy human donor (Hum). All mice were sacrificed on d8, 20 and 60 post-colonization in parallel to age-matched Cv and GF controls. RNA was extracted from ileal tissue, and processed to biotin-labelled cRNA, and then hybridized to the NuGO array (mouse) NuGO_Mm1a520177. Microarray analysis compared gene expression in ileum tissue of all the treatment groups GF, Cv, Cvd, Hum and SFB (N=3 per treatment group per time-point). Data was considered significant when P<0.05 using the Benjamini and Hochberg false discovery method.
2010-05-05 | E-GEOD-18056 | biostudies-arrayexpress
Project description:Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Using gnotobiotic mouse models, we provide a systematic analysis of the role of microbiota in the induction of cytokine responses in the normal intestine. Colonization by a whole mouse microbiota orchestrated a broad spectrum of pro-inflammatory (Th1, Th17) and regulatory T cell responses. Unexpectedly, most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal cytokine responses. A potent cytokine-inducing function was however associated with non-culturable host-specific species, the prototype of which was the Clostridia-related Segmented Filamentous Bacterium, and this bacterial species recapitulated the coordinated maturation of T cell responses induced by the whole mouse microbiota. Our study demonstrates the non-redundant role of microbiota members in the regulation of gut immune homeostasis.
2009-09-11 | GSE18056 | GEO
Project description:This pilot research trial studies the effects of chemotherapy on intestinal bacteria/organisms (microbiota) in patients newly diagnosed with breast cancer. Change in intestinal microbiota may be associated with weight gain in patients treated with chemotherapy. Weight gain has been also associated with cancer recurrence. Examining the types and quantity of bacterial composition in the stool of breast cancer patients treated with chemotherapy may help determine whether body weight and composition are associated with changes in the intestinal microbiota and allow doctors to plan better treatment to prevent weight gain and possibly disease recurrence.
| 2184354 | ecrin-mdr-crc
Project description:We developed a non-invasive ex vivo HT29 cell-based minimal model to fingerprint the mucosa-associated microbiota fraction in humans. HT29 cell-associated fractions were characterized by the universal phylogenetic array platform HTF-Microbi.Array, both in presence or in absence of a TNF-M-NM-1-mediated pro-inflammatory stimulus. A high taxonomical level fingerprint profiling of the mucosa-associated microbiota was performed on a group of 12 breast-fed infants and 6 adults (used as controls). Relative abundance of the bacterial species was assessed by using a so-called HTF-Microbi.Array, based on a ligation detection reaction (LDR) - Univerasal array (UA) assay, capable of correctly identify up to 31 intestinal bacterial groups, covering up to 95% of the human gut microbiota
2013-09-26 | E-GEOD-51177 | biostudies-arrayexpress
Project description:Bacterial species cultivated from multiple sites across the human microbiota (oral, nasal, skin, gastrointestinal tract, reproductive tract).
| PRJNA549513 | ENA
Project description:The emerging alphavirus chikungunya virus (CHIKV) has infected millions of people. However, the factors modulating disease outcome remain poorly understood. We show that depletion of the gut microbiota in oral antibiotic-treated or germ-free mice leads to greater CHIKV infection and spread within one day of virus inoculation. Perturbation of the gut microbiota alters TLR7-MyD88 signaling in plasmacytoid dendritic cells (pDCs) and blunts systemic production of type I interferon (IFN). Consequently, circulating monocytes express fewer IFN-stimulated genes and become permissive for CHIKV infection. Reconstitution with a single commensal bacterial species, Clostridium scindens, or its derived metabolite, the bile acid deoxycholic acid, can restore pDC- and MyD88-dependent type I IFN responses to restrict systemic CHIKV infection and transmission back to vector mosquitoes. Thus, commensal gut bacteria modulate antiviral immunity and levels of circulating alphaviruses within hours of infection through a bile acid-pDC-IFN signaling axis, which affects virus dissemination and potentially, epidemic spread
2020-05-13 | GSE150387 | GEO