Expression data for LGG exposure to C. elegnas
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans synthetic construct
PROVIDER: GSE190701 | GEO | 2021/12/12
REPOSITORIES: GEO
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Project description:Expression data for LGG exposure to C. elegnas
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Project description:Analysis of human primary macrophages after live Lactobacillus rhamnosus GG (LGG) or LC705 stimulation for 6h and 24h. The results reveal novel mechanisms for probiotics-induced activation of the healthy human innate immune system. Macrophages are phagocytic cells of the innate immune system that perform sentinel functions to initiate appropriate responses to surrounding stimuli. Macrophages that reside at mucosa encounter ingested bacteria. Our understanding of the responses elicited by nonpathogenic bacteria in human innate immune system is limited. Lactobacillus are nonpathogenic bacteria commonly used in food and as supplements with health-promoting probiotic potential. In this study, we have utilized global gene expression profiling to compare the responses of human primary macrophages to two closely related, well-characterized L. rhamnosus strains LGG and LC705. Our results demonstrate that live LGG and LC705 induced quantitatively different gene expression in macrophages. A gene ontology analysis revealed functional similarities and differences in responses to LGG and LC705. Both LGG and LC705 induced IL-1b production in macrophages that required caspase-1 activity. LC705 but not LGG induced a strong type I IFN-dependent gene activation that correlated with the ability of LC705 to prevent influenza A virus replication and production of viral proteins in macrophages. Differentiated 7d human primary macrophages from 18 healthy individuals were stimulated with either live L. rhamnosus GG (LGG) or LC705 for 6 h and 24 h in RPMI medium containing penicillin and streptomycin. As a control, macrophages were stimulated with the medium only. The experiment was performed three times, each time with cells from six different individuals (samples 1-3). For each experiment, macrophages were stimulated separately as described, and macrophages from different donors were pooled after each stimulation experiment. Extracted RNA was hybridized to AffymetrixM-BM-. U133-plus2.0 GeneChipM-BM-. arrays.
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Project description:YAMC (young adult mouse colon) cells are a conditionally immortalized mouse colonic intestinal epithelial cell line derived from the Immortimouse.Prior to each experiment, cells were plated at a density of 7.5 x 105 cells per p100mm dish.Cells were treated with LGG (the probiotic Lactobacillus GG ) conditioned media overnight, then harvested the following day. RNA were extracted with Trizol and purified with Qiagen kit. Affymetrix microarray chip Mouse 430A containing 19,000 murine genes was run in duplicate(experiment on 7-24-03 and 1-22-04 ). Data were analyzed using Affymetrix Genechip Operating Software (GCOS, Version 1.0) In each case; LGG treatment was compared to mock treatment controls. Results are expressed as fold change of treated cells as compared to controls, as calculated using GENESPRING software (Version 4.2.1, Silicon Genetics, Mountain View, CA), Statistical analysis was performed using D chip. DNA microarray experiments demonstrate that epithelial cell hsp70 is one of the most highly upregulated genes in response to LGG-CM treatment Keywords: repeat sample
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Project description:PM2.5 exposure induces lifespan reduction in Caenorhabditis elegans
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Project description:Analysis of human primary macrophages after live Lactobacillus rhamnosus GG (LGG) or LC705 stimulation for 6h and 24h. The results reveal novel mechanisms for probiotics-induced activation of the healthy human innate immune system. Macrophages are phagocytic cells of the innate immune system that perform sentinel functions to initiate appropriate responses to surrounding stimuli. Macrophages that reside at mucosa encounter ingested bacteria. Our understanding of the responses elicited by nonpathogenic bacteria in human innate immune system is limited. Lactobacillus are nonpathogenic bacteria commonly used in food and as supplements with health-promoting probiotic potential. In this study, we have utilized global gene expression profiling to compare the responses of human primary macrophages to two closely related, well-characterized L. rhamnosus strains LGG and LC705. Our results demonstrate that live LGG and LC705 induced quantitatively different gene expression in macrophages. A gene ontology analysis revealed functional similarities and differences in responses to LGG and LC705. Both LGG and LC705 induced IL-1b production in macrophages that required caspase-1 activity. LC705 but not LGG induced a strong type I IFN-dependent gene activation that correlated with the ability of LC705 to prevent influenza A virus replication and production of viral proteins in macrophages.
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Project description:To elucidate the molecular mechanism underlying lifespan reduction induced by PM2.5 exposure in Caenorhabditis elegans, we performed global gene expression profiling by RNA-sequencing technology, and compared the gene expression pattern change induced by PM2.5 exposure.
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Project description:Aging is under genetic control in C. elegans but the mechanisms of lifespan regulation are not completely known. MicroRNAs (miRNAs) regulate various aspects of development and metabolism and one miRNA has been previously implicated in lifespan. Here we show that multiple miRNAs change expression in C. elegans aging, including novel miRNAs, and that mutations in several of the most up-regulated miRNAs lead to lifespan defects. Some act to promote normal lifespan and stress resistance while others inhibit these phenomena. We find that these miRNAs genetically interact with genes in the DNA damage checkpoint response pathway and in the insulin signaling pathway. Our findings reveal that miRNAs both positively and negatively influence lifespan. Since several miRNAs up-regulated during aging regulate genes in conserved pathways of aging and thereby influence lifespan in C. elegans, we propose that miRNAs may play important roles in stress response and aging of more complex organisms. 4 sample examined: Wild-type (N2) and long-lived daf-2(e1379) animals at days 0 and 10 of adulthood
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Project description:Low-grade glioma (LGG) is a primary, slow-growing brain tumor; however, its treatment and prognosis remain challenging. In this study, we analyzed cancer data from the TCGA database, focusing particularly on the expression of the CDKN3 gene in LGG. The results showed that high CDKN3 expression in LGG patients was significantly associated with poor survival outcomes. Further gene expression analysis revealed that 379 genes were significantly upregulated in LGG samples with high CDKN3 expression, and these genes were primarily involved in the mitotic cell cycle and extracellular matrix organization. Additionally, high CDKN3 expression was closely linked to key signaling pathways such as tumor inflammation, hypoxic response, and tumor proliferation. Immune microenvironment analysis showed that high CDKN3 expression significantly increased the expression of CD4+ T cells and specific immune checkpoint genes, suggesting a potentially poor response to immune checkpoint blockade therapy. Through in vitro and in vivo experiments, we confirmed that CDKN3 silencing significantly inhibited the proliferative capacity of LGG cells. Proteomics revealed that CDKN3 can bind ARG1 and upregulate intracellular arginine concentrations. These findings not only improve our understanding of LGG biology but also provide scientific evidence for developing potential therapeutic strategies targeting CDKN3.
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Project description:Low-grade glioma (LGG) is a primary, slow-growing brain tumor; however, its treatment and prognosis remain challenging. In this study, we analyzed cancer data from the TCGA database, focusing particularly on the expression of the CDKN3 gene in LGG. The results showed that high CDKN3 expression in LGG patients was significantly associated with poor survival outcomes. Further gene expression analysis revealed that 379 genes were significantly upregulated in LGG samples with high CDKN3 expression, and these genes were primarily involved in the mitotic cell cycle and extracellular matrix organization. Additionally, high CDKN3 expression was closely linked to key signaling pathways such as tumor inflammation, hypoxic response, and tumor proliferation. Immune microenvironment analysis showed that high CDKN3 expression significantly increased the expression of CD4+ T cells and specific immune checkpoint genes, suggesting a potentially poor response to immune checkpoint blockade therapy. Through in vitro and in vivo experiments, we confirmed that CDKN3 silencing significantly inhibited the proliferative capacity of LGG cells. Proteomics revealed that CDKN3 can bind ARG1 and upregulate intracellular arginine concentrations. These findings not only improve our understanding of LGG biology but also provide scientific evidence for developing potential therapeutic strategies targeting CDKN3.
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