Genus Escherichia
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA339105 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4292310_1.fastq.gz | Fastqsanger.gz | |||
| SRR4292310_2.fastq.gz | Fastqsanger.gz | |||
| SRR4292311_1.fastq.gz | Fastqsanger.gz | |||
| SRR4292311_2.fastq.gz | Fastqsanger.gz | |||
| SRR4292312_1.fastq.gz | Fastqsanger.gz |
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Project description:Many human infections are polymicrobial in origin, and interactions among community inhabitants shape colonization patterns and pathogenic potential1. However, few interspecies interactions have been functionally dissected at the molecular level or characterized on a systems level. Periodontitis, which is the sixth most prevalent infectious disease worldwide2, ensues from the action of dysbiotic polymicrobial communities3. The keystone pathogen Porphyromonas gingivalis and the accessory pathogen Streptococcus gordonii interact to form communities in vitro and exhibit increased fitness in vivo3, 4. The mechanistic basis of this polymicrobial synergy, however, has not been fully elucidated. Here we show that streptococcal 4 aminobenzoate/para-amino benzoic acid (pABA) is required for maximal accumulation of P. gingivalis in dual species communities. Metabolomic and proteomic data showed that exogenous pABA is utilized for folate biosynthesis, and leads to decreased stress and elevated expression of fimbrial interspecies adhesins. Moreover, pABA increased the colonization and survival of P. gingivalis in a murine oral infection model. However, pABA also caused a reduction in virulence in vivo and suppressed extracellular polysaccharide production by P. gingivalis. Collectively, these data reveal a multidimensional aspect to P. gingivalis-S. gordonii interactions and establish pABA as a critical cue produced by a partner species that enhances fitness of P. gingivalis while diminishing virulence.
2017-09-26 | PXD006153 | Pride
Project description:Bacterial interspecies interactions shape the function and structural dynamics of microbial communities and affect disease progression of polymicrobial infections. Here, we present data suggesting that the FemA-FemR-FemI (Fem) cell surface signaling system in P. aeruginosa serves as an interspecies signaling pathway between P. aeruginosa and Mycobacterium species. The Fem system is regulated by the type three secretion system (T3SS) regulator ExsA. Fem system significantly influenced virulence factors in P. aeruginosa, including the quorum sensing systems, pyocyanin production, biofilm formation and the type six secretion systems (T6SSs). Our study using a Galleria mellonella infection model indicates femA deletion significantly increased the host survival rate while femI over-expression decreased it, demonstrating that the Fem system’s role in bacterial pathogenicity in vivo. We propose that the Fem system functions as an interspecies signaling pathway enabling P. aeruginosa to alter its behaviours in response to the presence of mycobacteria.
2021-01-14 | GSE164773 | GEO
Project description:Many human infections are polymicrobial in origin, and synergistic interactions among community inhabitants control colonization and pathogenic potential (Murray et al., 2014). However, few interspecies interactions have been functionally dissected at the molecular level or characterized on a systems level. Periodontitis, which is the sixth most prevalent infectious disease worldwide (Kassebaum et al., 2014), is associated with a dysbiotic microbial community, and the keystone pathogen Porphyromonas gingivalis forms synergistic communities with the accessory pathogen Streptococcus gordonii (Lamont and Hajishengallis, 2015). P. gingivalis and S. gordonii communicate through co-adhesion and metabolite perception, and close association between P. gingivalis and S. gordonii results in significant changes in the expressed proteomes of both organisms (Kuboniwa et al., 2012, Hendrickson et al., 2012). Here we show that streptococcal 4 aminobenzoate/para-amino benzoic acid (pABA) is required for maximal accumulation of P. gingivalis in communities with S. gordonii. Exogenous pABA upregulates production of fimbrial interspecies adhesins and of a tyrosine phosphorylation-dependent signaling system in P. gingivalis. Consequently, fimbrial-dependent attachment and invasion of epithelial cells by P. gingivalis is also increased by pABA. Moreover, trans-omics studies performed by proteomics and metabolomics showed that pABA induces metabolic shifts within P. gingivalis, predominantly folate derivative biosynthesis. In a murine oral infection model, pABA increased colonization and survival of P. gingivalis, but did not increase virulence. The results establish streptococcal pABA as a major component of the interspecies S. gordonii-P. gingivalis interaction which regulates distinct aspects of polymicrobial synergy.
2016-04-16 | ST000384 | MetabolomicsWorkbench
Project description:NF-kB is a transcriptional factor that consists in homo and heterodimers of the large family of Rel subunits. Among the most important functions for NF-kB, initiation of immunological/inflammatory responses and regulation of cell proliferation/apoptosis which are the major features of severe infections. Although the role of NF-kB is crucial in host defense against pathogens, mice deficient for individual subunits of NF-kB have not been explored in murine models of polymicrobial infection. In this report, we have investigated in vivo the consequences of cRel subunit deficiency in the survival to polymicrobial infection. We have also approached the underlying mechanisms of the host defense by analyzing cytokine production, bacterial clearance and the distribution of innate and adaptive immune cells. Absence of cRel enhances mice mortality to polymicrobial sepsis. The decreased survival of cRel-/- animals upon infection is not related to altered local mechanisms of innate defense such as the peritoneal recruitment of the Gr.1+CD11b+ phagocytic cells and the bacterial clearance. However, cRel deficiency allows to altered systemic cytokine response associated to sustained loss of the lymphoïd subset CD8a+ of spleen dendritic cells, key antigen-presenting cells for the initiation of the adaptive immunity. Genome-wide analysis of the systemic host response to polymicrobial sepsis reveals inflammatory/immune and apoptotic gene signatures associated to cRel subunit. In this study we identified the NF-kB member cRel, as a key factor which plays a critical role in survival to polymicrobial sepsis and also as a regulatory transcription subunit controlling the inflammatory and the adaptive immune responses in severe infection.
2011-10-14 | E-MEXP-2944 | biostudies-arrayexpress
Project description:Infection is able to elicit innate immunological memory by enhancing a long-term myeloid output even after the inciting infectious agent has been cleared. However, mechanisms underlying such a regulation are not fully understood. Using a mouse polymicrobial peritonitis (sepsis) model, we show that severe infection leads to increased, sustained myelopoiesis after the infection is resolved. The infection experience is imprinted in the bone marrow (BM) stromal cells, in the form of a constitutive upregulation of the tissue inhibitor of metalloproteinases 1 (TIMP1). TIMP1 antagonizes the function of ADAM10, an essential cleavage enzyme for the activation of Notch which in turn suppresses myelopoiesis. While TIMP1 is dispensable for myelopoiesis under the steady state, increased TIMP1 enhances myelopoiesis post infection. Thus, our data reveal that infection could establish an inflammatory memory in the BM niche to support a long-term enhanced output of innate immune cells.
2022-06-15 | GSE205728 | GEO
Project description:To investigate the importance of IL-3 during the pulmonary response to HSV infection after initial polymicrobial sepsis
2023-02-08 | GSE224299 | GEO
Project description:Acute phase proteins (APPs) are an evolutionarily conserved family of proteins produced mainly in the liver in response to infection and inflammation. Despite vast pro- and anti-inflammatory properties ascribed to individual APPs, their collective function during infections remains poorly defined. Using a murine model for polymicrobial sepsis we show here that abrogation of APP production by hepatocyte-specific gp130 deletion, the signaling receptor shared by IL-6-family cytokines, dramatically increased mortality despite normal bacterial clearance. Hepatic gp130 signaling through signal transducer and activator of transcription (Stat)3 was required to control systemic inflammation. Notably, hepatic gp130/Stat3 activation was also a prerequisite to facilitate mobilization and tissue accumulation of myeloid-derived suppressor cells (MDSCs), a cell population mainly known for anti-inflammatory properties in cancer. We show that MDSCs were critical to regulate innate inflammation and their adoptive transfer efficiently protected gp130-deficient mice from sepsis-associated mortality. We identified serum amyloid A and Cxcl-1/KC as hepatic acute phase genes that cooperatively promoted MDSC mobilization, accumulation and survival. Administration of these proteins efficiently elevated MDSC numbers and reversed dysregulated inflammation and restored survival of gp130-deficient mice. Thus, gp130-dependent communication between the liver and MDSCs through acute phase proteins critically controls inflammatory responses during infection. Control [gp130f/f] and liver-specific Gp130 knockout [gp130delta(hepa)] mice were subjected to polymicrobial sepsis. Twelve hours after induction of sepsis mice were sacrificed and livers were removed. For control treatment mice were sacrified without any prior treatment. Total RNA was isolated and subjected to gene expression profiling.
2010-06-08 | E-GEOD-22009 | biostudies-arrayexpress
Project description:we develop an interspecies pluripotent stem cell (PSC) co-culture strategy and uncover a previously unknown mode of cell competition. Interspecies PSC competition occurs during primed but not naive pluripotency, and between evolutionarily distant species. We identified genes related to NF-κB signaling pathways, among others, were upregulated in loser cells and genetic inactivation of RELA, a core component of canonical NF-κB pathway, could overcome interspecies PSC competition. We further showed that an upstream regulator of the NF-κB signaling, MYD88 innate immune signal transduction adaptor, was also involved in promoting loser PSC elimination. Suppressing interspecies PSC competition via genetic perturbation of MYD88 or P65 improved engraftment of human cells in early post-implantation mouse embryos. Our study discovers a new paradigm of cell competition and paves the way for studying evolutionarily conserved cell competition mechanisms during early mammalian development. Strategies developed here to overcome interspecies PSC competition may facilitate interspecies organogenesis between evolutionary distant species, including humans.
2020-12-31 | GSE142394 | GEO
Project description:To describe the transcriptional changes associated with polymicrobial-sepsis induced myocardial depression in wild type and iNOS deficient mice. Keywords: myocardium, contractility, differential gene expression, nitric oxide synthase, infection
2010-11-17 | GSE9667 | GEO