Project description:Different attB or attP DNA libraries containing 7-bp random nucleotides were used for in vitro recombination mediated by the purified integrase from mv4 bacteriophage against their cognate wild-type attB or attP recombination site.
Project description:Impairment of the intestinal barrier allows the systemic translocation of commensal bacteria, inducing a pro-inflammatory state in the host. To explore this link, we investigated innate immune responses following increased gut permeability upon administration of dextran sulfate sodium (DSS) in mice. We found that microbiota translocation induced trained immunity (TI) in mouse myeloid bone marrow progenitors (BMPs). Enterococcus faecalis was isolated from bone marrow following DSS treatment and induced trained immunity hallmarks in bone marrow-derived mouse macrophages and human monocytes. Notably, DSS treatment or heat-killed E. faecalis reprogrammed BMPs, resulting in enhanced inflammatory responses in vitro and in vivo, and protection against pathogen infections. The C-type lectin receptor Mincle (Clec4e) was essential for E. faecalis-induced TI in BMPs. Clec4e-/- mice showed impaired TI upon E. faecalis and reduced pathology following DSS treatment. Thus, Mincle sensing of E. faecalis induces TI that may contribute to pathologies associated with increased gut permeability. This SuperSeries is composed of the SubSeries listed below.
2025-01-22 | GSE281377 | GEO
Project description:Bacteriophages against Enterecoccus faecalis
Project description:The neuronal G protein-coupled receptor NMUR-1, a homolog to the mammalian neuromedin U receptor, has been implicated in the specificity of Caenorhabditis elegans innate immune response against pathogen infections. NMUR-1 controls C. elegans transcription activity by regulating transcription factors, which, in turn control the expression of distinct defense genes. This study further investigates the role of NMUR-1 at the protein level in regulating innate immune responses against pathogens Salmonella enterica and Enterococcus faecalis by utilizing mass spectrometry-based quantitative proteomics. We found that NMUR-1 regulates a class of proteins responsible for transmembrane transport during infection. Specifically, a group of proteins forming F1FO ATP synthase responsible for ATP biosynthesis is downregulated in NMUR-1 loss of function mutants during both S. enterica and E. faecalis infections. ATP measurements further revealed that nmur-1 mutants have reduced ATP production in response to both S. enterica and E. faecalis infections. Functional assays demonstrated that inhibiting F1FO ATP synthase using RNA interference or chemical modification mimicked the survival phenotypes of the untreated nmur-1 knockout mutants on S. enterica and E. faecalis. These findings provide valuable insights into the mechanism by which NMUR-1 regulates energy homeostasis at the protein level as part of an innate immune response against specific pathogens.