Bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB18874 | ENA |
REPOSITORIES: ENA
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Project description:Skin bacteria impact melanoma related pathways Melanoma represents the most lethal form of skin cancer, with rising numbers of annual incidences worldwide. In an effort to identify new risk factors that promote melanoma development, the contribution of the skin microbiome gained increasing attention. Previous studies already demonstrated an altered composition of the skin microbiome on melanoma sites. Yet, the underlying mechanisms of the interplay between the microbiome and melanoma progression remain elusive. We established a novel co-culture system capable to study host microbiome interactions during melanoma progression in situ. This system consists of a commercial 3D melanoma skin model colonized with skin bacteria obtained from a skin swab of a healthy volunteer. The models showed a stable co-colonization over a period of 12 days, with Streptococcus being the most abundant genus on the last day of cultivation. Transcriptome profiles revealed significant differences in colonized models compared to control. In particular, pathways involved in melanoma progression, like RAF/MAP and PI3K kinase, were upregulated in colonized models. This correlates with the augmented release of the cytokines VEGF, PIGF, and GM-CSF as well as the typical melanoma markers MIA and S100B. Furthermore, the data were supported by an active epithelial-mesenchymal transition in colonized skin models. Taken together, the bacterial community seems to promote the progression of melanoma in our established system, hence we provide an elegant method to elucidate the microbiome’s impact on cancer development in situ.
2026-02-17 | GSE273669 | GEO
Project description:Microsporidium that is clinically significant
| PRJNA21013 | ENA
Project description:clinically significant Nocardia species (PRJCA018008)
| PRJDB36178 | ENA
Project description:Objectives: To define the inflammatory signature of healthy keratinocytes induced by gram-negative anaerobe bacteria commonly found in HS and investigate pathways of activation. Methods: Type strains of P. nigrescens, P. melanogenica, P. intermedia, P. asaccharolytica, F. nucleatum, as well as S. aureus and the normal skin commensal S. epidermidis were heat-killed and co-incubated with normal human keratinocytes. RNA was analyzed using RNAseq and RT-qPCR. TLR4 and JAK inhibitors were used to investigate mRNA and protein inhibition of inflammatory cytokines. Results: All GNAs tested induced significantly higher levels of CXCL8 than S. epidermidis or negative control. P. nigrescens, P. melanogenica, and F. nucleatum were the most stimulatory and produced CXCL8 levels much higher than S. aureus. RNASeq revealed a broad inflammatory profile most strongly induced by F. nucleatum. All three bacteria strongly activated the IL-17 pathway and correlated with HS skin transcriptomes. Both TLR4 and JAK inhibition significantly reduced keratinocyte inflammation. Results: All GNAs tested induced significantly higher levels of CXCL8 than S. epidermidis or negative control. P. nigrescens, P. melanogenica, and F. nucleatum were the most stimulatory and produced CXCL8 levels much higher than S. aureus. RNASeq revealed a broad inflammatory profile most strongly induced by F. nucleatum. All three bacteria strongly activated the IL-17 pathway and correlated with HS skin transcriptomes.
2024-06-30 | GSE237052 | GEO
Project description:Type 1 diabetes (T1D) is a chronic autoimmune disease that results from destruction of pancreatic β-cells. T1D subjects were recently shown to harbor distinct intestinal microbiome profiles. Based on these findings, the role of gut bacteria in T1D is being intensively investigated. The mechanism connecting intestinal microbial homeostasis with the development of T1D is unknown. Specific gut bacteria such as Bacteroides dorei (BD) and Ruminococcus gnavus (RG) show markedly increased abundance prior to the development of autoimmunity. One hypothesis is that these bacteria might traverse the damaged gut barrier, and their constituents elicit a response from human islets that causes metabolic abnormalities and inflammation. We have tested this hypothesis by exposing human islets to BD and RG in vitro, after which RNA-Seq analysis was performed. The bacteria altered expression of many islet genes. The commonly upregulated genes by these bacteria were cytokines, chemokines and enzymes, suggesting a significant effect of gut bacteria on islet antimicrobial and biosynthetic pathways. Additionally, each bacteria displayed a unique set of differentially expressed genes (DEGs). Ingenuity pathway analysis of DEGs revealed that top activated pathways and diseases included TREM1 Signaling and Inflammatory Response, illustrating the ability of bacteria to induce islet inflammation. The increased levels of selected factors were confirmed using immunoblotting and ELISA methods. Our data demonstrate that islets produce a complex anti-bacterial response. The response includes both symbiotic and pathogenic aspects. Both oxidative damage and leukocyte recruitment factors were prominent, which could induce beta cell damage and subsequent autoimmunity.
2019-10-30 | GSE131320 | GEO
Project description:Here, we report significant changes in the composition of the lung microbiome and metabolome of mice under immune suppression, infection of immunosuppressed mice with virulent and avirulent strains of the clinically important human-pathogenic fungus Aspergillus fumigatus, and treatment with the clinically used antifungal drug voriconazole. Our data also indicate the important role of the gut microbiome for the lung homeostasis mediated by the plasma metabolome. In the lung microbiome, infection by A. fumigatus led to a significant increase of anaerobic bacteria, most prominently of Ligilactobacillus murinus. We also isolated live bacteria including L. murinus from the murine lower respiratory tract. In vitro, L. murinus is tolerated and even internalized by alveolar epithelial cells. Co-cultivation of L. murinus and A. fumigatus led to a reduction in oxygen concentration accompanied by an increase of L. murinus cells suggesting that A. fumigatus establishes a microaerophilic niche, thereby promoting growth of anaerobic bacteria.
2025-07-04 | MTBLS12262 | MetaboLights