Ontology highlight
ABSTRACT:
PROVIDER: PRJNA540393 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8992020_1.fastq.gz | Fastqsanger.gz | |||
| SRR8992020_2.fastq.gz | Fastqsanger.gz | |||
| SRR8992030_1.fastq.gz | Fastqsanger.gz | |||
| SRR8992030_2.fastq.gz | Fastqsanger.gz | |||
| SRR8992021_1.fastq.gz | Fastqsanger.gz |
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Project description:Skin-resident Staphylococcus aureus, a common human commensal, can shape systemic immune responses without provoking inflammation in mice. This study demonstrates that topical skin colonization with live S. aureus robustly expands IL-17-producing Vγ6⁺ γδT17 cells both locally in the dermis and across distant tissues, including mucosal, lymphoid, and metabolic organs. This systemic reconfiguration is IL-1R-dependent yet independent of IL-23, TLR2, or the microbiota. Transcriptomic profiling reveals a transitional state in dermal Vγ6⁺ γδT cells, marked by changes in tissue-residency and migration-associated genes. Local proliferation, lymphatic trafficking and long-term recirculation sustain this response, even without systemic bacterial dissemination. These findings uncover a previously unrecognized allostatic process by which localized microbial signals recalibrate systemic immunological setpoints. The study expands our understanding of γδT17 cell dynamics and highlights their potential in tuning organismal fitness.
2026-04-01 | GSE294609 | GEO
Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils. Lesional skin biopsies obtained from C57BL/6J WT mice or IL-1R-deficient mice at 4 hours post-infection with Staphylococcus aureus. Uninfected skin biopsies were also collected from WT and IL-1R-deficient mice.
2012-12-05 | E-GEOD-36826 | biostudies-arrayexpress
Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.
2012-12-05 | GSE36826 | GEO
Project description:The complex system by which the skin regulates immune responses to the external environment is unclear. Here, we investigated cell-cell interactions underlying cutaneous defense against S. aureus. Single-cell transcriptomics (scRNA-Seq) and unbiased network analysis revealed unexpected, dominant IL-17-mediated dermal reticular fibroblast-to-neutrophil communication. Multi-faceted in vitro omics studies demonstrated that IL-17 synergized with several factors including TNF⍺ to induce fibroblast NFKBIZ and chemokine secretion. Cultured fibroblasts drove robust neutrophil recruitment through NFKBIZ-dependent CXCR2 and CXCR4 ligands. Mice lacking IL-17R in fibroblasts (PdgfraΔIl17ra) were generated to determine the significance of fibroblast-neutrophil communication. PdgfraΔIl17ra mice exhibited drastically reduced skin neutrophilia in multiple disease models and reduced defense against S. aureus. These findings were translated to humans by comprehensive analysis of biopsies from psoriasis patients on and off anti-IL-17 treatment. Thus, dermal fibroblasts are critical for skin type 17 inflammation and represent a novel target for treatment of infection and inflammatory disease.
2024-02-14 | GSE230511 | GEO
Project description:The complex system by which the skin regulates immune responses to the external environment is unclear. Here, we investigated cell-cell interactions underlying cutaneous defense against S. aureus. Single-cell transcriptomics (scRNA-Seq) and unbiased network analysis revealed unexpected, dominant IL-17-mediated dermal reticular fibroblast-to-neutrophil communication. Multi-faceted in vitro omics studies demonstrated that IL-17 synergized with several factors including TNF⍺ to induce fibroblast NFKBIZ and chemokine secretion. Cultured fibroblasts drove robust neutrophil recruitment through NFKBIZ-dependent CXCR2 and CXCR4 ligands. Mice lacking IL-17R in fibroblasts (PdgfraΔIl17ra) were generated to determine the significance of fibroblast-neutrophil communication. PdgfraΔIl17ra mice exhibited drastically reduced skin neutrophilia in multiple disease models and reduced defense against S. aureus. These findings were translated to humans by comprehensive analysis of biopsies from psoriasis patients on and off anti-IL-17 treatment. Thus, dermal fibroblasts are critical for skin type 17 inflammation and represent a novel target for treatment of infection and inflammatory disease.
2024-02-15 | GSE230512 | GEO
Project description:One common way to classify functional γδ T cell subsets is based on the expressed variable gene region of the T-cell-receptor (TCR) γ-chain. It is established that the TCRs of murine IL-17 producing γδ T cells are either Vγ6+ or Vγ4+. The majority of IL-17 producers get functionally pre-programmed in the prenatal thymus, and persist thereafter as tissue-resident cells into adulthood. Little is known about the role of the expressed TCR on IL-17 effector fate acquisition, and if also other subsets can produce IL-17 under certain circumstances. To address this question, we took advantage of a mouse model that lack the Vγ4 and Vγ6 γ-chain (Vγ4-/- / Vγ6-/- double knock-out). Initial results indicate that Vγ1+ T cells show increased IL-17 production capability in the absence of Vγ4+ and Vγ6+ γδ T cells, suggesting that the γδTCR does not always instruct the phenotype. This raises the question about the ontogenetic origin, which might be a TCR-independent default mechanism to instruct IL-17 production by γδ T cells, of IL-17+ Vγ1+ T cells. Moreover, it remains elusive if these Vγ1+ T cells (i) adopt highly similar tissue-specific gene expression programs and (ii) functionality in health and disease, than the Vγ4+ and Vγ6+ T cells.
2025-09-24 | GSE284167 | GEO
Project description:One common way to classify functional γδ T cell subsets is based on the expressed variable gene region of the T-cell-receptor (TCR) γ-chain. It is established that the TCRs of murine IL-17 producing γδ T cells are either Vγ6+ or Vγ4+. The majority of IL-17 producers get functionally pre-programmed in the prenatal thymus, and persist thereafter as tissue-resident cells into adulthood. Little is known about the role of the expressed TCR on IL-17 effector fate acquisition, and if also other subsets can produce IL-17 under certain circumstances. To address this question, we took advantage of a mouse model that lack the Vγ4 and Vγ6 γ-chain (Vγ4-/- / Vγ6-/- double knock-out). Initial results indicate that Vγ1+ T cells show increased IL-17 production capability in the absence of Vγ4+ and Vγ6+ γδ T cells, suggesting that the γδTCR does not always instruct the phenotype. This raises the question about the ontogenetic origin, which might be a TCR-independent default mechanism to instruct IL-17 production by γδ T cells, of IL-17+ Vγ1+ T cells. Moreover, it remains elusive if these Vγ1+ T cells (i) adopt highly similar tissue-specific gene expression programs and (ii) functionality in health and disease, than the Vγ4+ and Vγ6+ T cells.
2025-09-24 | GSE284198 | GEO
Project description:Skin commensal bacteria (Staphylococcus epidermidis) can help defend against skin infections, and they are increasingly being recognized for their role in benefiting skin health. This study aims to demonstrate the activities that Myristica fragrans Houtt. seed extracts, crude extract (CE) and essential oil (EO), have in terms of promoting the growth of the skin commensal bacterium S. epidermidis and providing metabolites under culture conditions to disrupt the biofilm formation of the common pathogen Staphylococcus aureus.
2025-09-01 | PXD055409 | JPOST Repository
Project description:Background: Atopic dermatitis (AD) is a common inflammatory skin disease with a TH2 immune polarity and is often colonized with Staphylococcus aureus. Despite recent advances in understanding Staphylococcus species infection and the impact of polar TH cytokines on the skin, the interactions between these factors in AD pathology are poorly understood. Methods: AD-related key immune biomarkers were measured by quantitative real-time PCR in human keratinocytes exposed heat-killed S. epidermidis or S. aureus with/without polar T-cell derived cytokines such as IFN-γ (TH1), IL-4/IL-13 (TH2), and IL-22 (TH22). Further analysis was performed by RNA-sequencing to define broader responses in both Staphylococcus species and polar cytokines. The similarity of gene expression patterns in AD skin lesions and stimulated keratinocytes was evaluated by gene-set variation analysis (GSVA). Results: Gene expression analysis exhibited distinct immune responses in keratinocytes depending on individual bacterial or polar cytokine exposure. Besides, numerous genes were synergistically upregulated by the combination exposure of bacteria and polar TH cytokines. Moreover, GSVA revealed that combined exposure of S. aureus and IL-4 + IL-13 exhibited significantly higher correlations with a genomic signature of AD skin lesions than their single exposure or combinations of other polar TH cytokines. Conclusions: Our findings provide novel insights into AD-related transcriptional activation and illustrate a potentially novel pathogenic function of S. aureus and IL-4/IL-13 interactions in AD.
2021-12-31 | GSE173902 | GEO
Project description:γδ T cells producing interleukin 17A (IL-17A), which are mainly Vγ4 and Vγ6 subsets, are involved in protection against infection by extracellular bacteria. Using a new Vγ6-specific monoclonal antibody (mAb) (1C10-1F7) which we recently developed, we found that IL-17A+ Vγ6+ γδ T cells increased predominantly in the peritoneal cavity compared with IL-17A+ Vγ4+ γδ T cells during intraperitoneal Escherichia coli infection. The number of IL-17A+ Vγ6+ γδ T cells, which rapidly became CD69+ from CD69-, peaked at 12 h after infection. In vivo treatment with 1C10-1F7 mAb significantly inhibited the accumulation of neutrophils and hampered the resolution of E. coli infection. These results suggest that rapid activation of IL-17A+ Vγ6+ γδ T cells contributed to host defence against E. coli infection.
2020-02-28 | GSE144617 | GEO