Microbes in flotation
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB66423 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Microbes are an integral component of the tumor microenvironment (TME). However, mechanisms that direct microbial recruitment into tumors and the spatial relationship between intratumoral microbes and host cells remain poorly understood. Here, we show that microbes and immune cells have parallel spatial distribution and that the presence of intratumoral microbes is dependent on T cells. Analysis of human pancreatic ductal adenocarcinomas (PDAC) and lung adenocarcinomas (LUAD) revealed a spatially heterogeneous distribution of lipopolysaccharide (LPS) that is associated with T cell infiltration. Using mouse models of PDAC, we found that microbes were more abundant and diverse in tumors that were enriched in T cells compared to tumors that lacked T cells, despite no significant differences in the fecal microbiome. Consistent with these findings, we detected elevated levels of microbial genes in T cell-enriched tumor nests in human PDAC. Compared to microbe-poor tumor nests, microbe-enriched tumor nests displayed a higher number of myeloid cells, B cells, and plasma cells. Microbe-enriched tumor nests also showed upregulation of immune-related processes, including responses to bacteria, and receptors that mediate mucosal immune responses to microbes. Administration of antibiotics to tumor-bearing mice altered the phenotype and presence of intratumoral myeloid cells and B cells but did not alter T cell infiltration. In contrast, depletion of T cells reduced the presence of intratumoral microbes. Our results identify a novel coupling between microbes and the intratumoral immune landscape, with T cells shaping microbial presence and subsequent microbial-host interactions.
2023-12-01 | GSE213736 | GEO
Project description:This study examines the role of early exposure to gut microbes and poor diet on microglial function in mice. Groups = control (CON), malnourished (MAL), and malnourished + microbial exposure (E/MALBG). CD11b+ cells (microglial enrichment) were isolated from whole mouse brains (Adult Brain Disruption Kit, Miltenyi Biotec). After sample quality control (Agilent 2100 Bioanalyzer), qualifying samples were sent for RNA-Seq (Illumina NextSeq 500 with Paired End 42bp × 42bp reads; demultiplexed: Illumina's bcl2fastq2). Following alignment against mouse reference genes (STAR aligner), DEG analyses was conducted using the DESeq2 pipeline.
2021-05-31 | GSE138182 | GEO
Project description:Solid tumors are composed of cancer cells and host immune cells that are distributed in a non-uniform pattern. Growing evidence shows that intratumoral microbes are associated with immune microenvironments in cancer. However, mechanisms that direct the recruitment of microbes to tumors remain poorly understood. Here, we show that intratumoral infiltration of immune cells and microbes are heterogeneous, and the distribution of microbes within tumors are orchestrated by the spatial heterogeneity of intratumoral lymphoid populations. Analysis of human solid tumors revealed that the spatial distribution of immune cells, particularly CD8+ T cells, is markedly heterogeneous. Compared to T cell-poor (“cold”) tumor nests, T cell-rich (“hot”) tumor nests displayed a significantly higher number of myeloid cells, B cells, and plasma cells. We performed laser capture microdissection (LCM) followed by RNA sequencing to identify unique gene signatures that define tumor epithelium and stroma of cold and hot tumor nests. Cold tumor nests expressed genes that promote tumor proliferation and fibrosis, whereas hot tumor stroma and epithelium showed upregulation of immune-related processes, including responses to bacteria, and receptors that mediate mucosal immune responses to microbes, respectively. Consistent with these findings, we detected elevated levels of microbes within hot tumor nests in human pancreatic and lung cancers as well as in mouse models of pancreatic cancer. Intratumoral T cell infiltration plays a causal role in spatial distribution of bacteria in tumor. Our data implicate intratumoral immune heterogeneity in defining microbial spatial distribution and highlight a potential role for crosstalks between microbes, cancer cells, and the host immune system in shaping constituents of the tumor microenvironment (TME).
2023-12-01 | GSE189925 | GEO
Project description:Solid tumors are composed of cancer cells and host immune cells that are distributed in a non-uniform pattern. Although this spatial heterogeneity may reflect mutational variations in cancer cells, mechanisms that direct the recruitment of immune cells to distinct regions within a tumor remain poorly understood. Here, we show that microbial-host interactions define tumor nests enriched in immune cells, and the distribution of microbes within tumors parallels the spatial heterogeneity of intratumoral lymphoid and myeloid cell populations. Analysis of human solid tumors revealed that the spatial distribution of immune cells, particularly CD8+ T cells, is markedly heterogeneous. Compared to T cell-poor (“cold”) tumor nests, T cell-rich (“hot”) tumor nests displayed a significantly higher number of myeloid cells, B cells, and plasma cells. We performed laser capture microdissection (LCM) followed by RNA sequencing to identify unique gene signatures that define tumor epithelium and stroma of cold and hot tumor nests. Cold tumor nests expressed genes that promote tumor proliferation and fibrosis, whereas hot tumor stroma and epithelium showed upregulation of immune-related processes, including responses to bacteria, and receptors that mediate mucosal immune responses to microbes, respectively. Consistent with these findings, we detected elevated levels of microbes within hot tumor nests in human pancreatic and lung cancers. Our data implicate host immune responses to microbes in defining intratumoral immune heterogeneity and highlight a potential role for crosstalks between microbes, cancer cells, and the host immune system in regulating cancer immunogenicity.
2023-12-01 | GSE155723 | GEO
Project description:Solid tumors are composed of cancer cells and host immune cells that are distributed in a non-uniform pattern. Although this spatial heterogeneity may reflect mutational variations in cancer cells, mechanisms that direct the recruitment of immune cells to distinct regions within a tumor remain poorly understood. Here, we show that microbial-host interactions define tumor nests enriched in immune cells, and the distribution of microbes within tumors parallels the spatial heterogeneity of intratumoral lymphoid and myeloid cell populations. Analysis of human solid tumors revealed that the spatial distribution of immune cells, particularly CD8+ T cells, is markedly heterogeneous. Compared to T cell-poor (“cold”) tumor nests, T cell-rich (“hot”) tumor nests displayed a significantly higher number of myeloid cells, B cells, and plasma cells. We performed laser capture microdissection (LCM) followed by RNA sequencing to identify unique gene signatures that define tumor epithelium and stroma of cold and hot tumor nests. Cold tumor nests expressed genes that promote tumor proliferation and fibrosis, whereas hot tumor stroma and epithelium showed upregulation of immune-related processes, including responses to bacteria, and receptors that mediate mucosal immune responses to microbes, respectively. Consistent with these findings, we detected elevated levels of microbes within hot tumor nests in human pancreatic and lung cancers. Our data implicate host immune responses to microbes in defining intratumoral immune heterogeneity and highlight a potential role for crosstalks between microbes, cancer cells, and the host immune system in regulating cancer immunogenicity.
2023-12-01 | GSE155722 | GEO
Project description:Solid tumors are composed of cancer cells and host immune cells that are distributed in a non-uniform pattern. Although this spatial heterogeneity may reflect mutational variations in cancer cells, mechanisms that direct the recruitment of immune cells to distinct regions within a tumor remain poorly understood. Here, we show that microbial-host interactions define tumor nests enriched in immune cells, and the distribution of microbes within tumors parallels the spatial heterogeneity of intratumoral lymphoid and myeloid cell populations. Analysis of human solid tumors revealed that the spatial distribution of immune cells, particularly CD8+ T cells, is markedly heterogeneous. Compared to T cell-poor (“cold”) tumor nests, T cell-rich (“hot”) tumor nests displayed a significantly higher number of myeloid cells, B cells, and plasma cells. We performed laser capture microdissection (LCM) followed by RNA sequencing to identify unique gene signatures that define tumor epithelium and stroma of cold and hot tumor nests. Cold tumor nests expressed genes that promote tumor proliferation and fibrosis, whereas hot tumor stroma and epithelium showed upregulation of immune-related processes, including responses to bacteria, and receptors that mediate mucosal immune responses to microbes, respectively. Consistent with these findings, we detected elevated levels of microbes within hot tumor nests in human pancreatic and lung cancers. Our data implicate host immune responses to microbes in defining intratumoral immune heterogeneity and highlight a potential role for crosstalks between microbes, cancer cells, and the host immune system in regulating cancer immunogenicity.
2023-12-01 | GSE155724 | GEO
Project description:The mechanisms whereby enteric pathogens and microbes induce systemic antibody responses remain obscure. In contrast to accepted models, we show that commensal microbes have a dramatic impact on the bone marrow (BM) plasma cell pool. Unlike standard vendor mice, in mice reared in our colony the majority of long-lived BM plasma cells secreted IgA antibodies. Exposing vendor mice to a unique microflora or Helicobacter sp. led to the generation of IgA-secreting BM cells, while also inducing increases in serum IgA antibodies enriched for binding to several commensal bacterial taxa. Moreover, BM IgA-secreting plasma cells exhibited a common clonal ancestry with intestinal IgA+ plasma cells, and both populations possessed unique gene expression signatures compared to other long-lived BM plasma cells. We conclude that commensal microbes overtly influence the BM plasma cell pool, and suggest that select commensal microbes can facilitate the induction of systemic humoral immunity.
2018-07-01 | GSE87091 | GEO
Project description:Microbes Malnutrition Microglia
| PRJNA575001 | ENA