Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1273279 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To explore the regulatory mechanism of intestinal flora in Citrobacter rodentium -induced intestinal infection by transcriptome analysis at miRNA molecular level.
2024-03-04 | GSE260446 | GEO
Project description:Interventions: Kefir intake group(4 to 12 weeks)
Kefir long-term intake group (5 years)
Non-intake group
Primary outcome(s): Changes of the oral flora and intestinal flora Changes in the immune markers such as cell-mediated immunity Response Evaluation Criteria in Solid Tumors Overall survival time, Progression-free survival
Study Design: Parallel Randomized
| 2639154 | ecrin-mdr-crc
Project description:Recent studies demonstratethat inflammatory signals regulate hematopoietic stem cells (HSCs). Granulocyte-colony stimulating factor (G-CSF) is often induced with infection and plays a key role in the stress granulopoiesis response. However, its effects on HSCs are less clear. Herein, we show that treatment with G-CSF induces expansion and increased quiescence of phenotypic HSCs, but causes a marked, cell-autonomous HSC repopulating defect associated with induction of toll-like receptor (TLR) expression and signaling. The G-CSF-mediated expansion of HSCs is reduced in mice lacking TLR2, TLR4 or the TLR signaling adaptor MyD88. Induction of HSC quiescence is abrogated in mice lacking MyD88 or in mice treated with antibiotics to suppress intestinal flora. Finally, loss of TLR4 or germ free conditions mitigates the G-CSF-mediated HSC repopulating defect. These data suggest that low level TLR agonist production by commensal flora contributes to the regulation of HSC function and that G-CSF negatively regulates HSCs, in part, by enhancing TLR signaling.
2014-02-19 | GSE55094 | GEO
Project description:Recent studies demonstrate that inflammatory signals regulate hematopoietic stem cells (HSCs). Granulocyte-colony stimulating factor (G-CSF) is often induced with infection and plays a key role in the stress granulopoiesis response. However, its effects on HSCs are less clear. Herein, we show that treatment with G-CSF induces expansion and increased quiescence of phenotypic HSCs, but causes a marked, cell-autonomous HSC repopulating defect associated with induction of toll-like receptor (TLR) expression and signaling. The G-CSF-mediated expansion of HSCs is reduced in mice lacking TLR2, TLR4 or the TLR signaling adaptor MyD88. Induction of HSC quiescence is abrogated in mice lacking MyD88 or in mice treated with antibiotics to suppress intestinal flora. Finally, loss of TLR4 or germ free conditions mitigates the G-CSF-mediated HSC repopulating defect. These data suggest that low level TLR agonist production by commensal flora contributes to the regulation of HSC function and that G-CSF negatively regulates HSCs, in part, by enhancing TLR signaling.
2014-02-19 | GSE55093 | GEO
Project description:Recent studies demonstrate that inflammatory signals regulate hematopoietic stem cells (HSCs). Granulocyte-colony stimulating factor (G-CSF) is often induced with infection and plays a key role in the stress granulopoiesis response. However, its effects on HSCs are less clear. Herein, we show that treatment with G-CSF induces expansion and increased quiescence of phenotypic HSCs, but causes a marked, cell-autonomous HSC repopulating defect associated with induction of toll-like receptor (TLR) expression and signaling. The G-CSF-mediated expansion of HSCs is reduced in mice lacking TLR2, TLR4 or the TLR signaling adaptor MyD88. Induction of HSC quiescence is abrogated in mice lacking MyD88 or in mice treated with antibiotics to suppress intestinal flora. Finally, loss of TLR4 or germ free conditions mitigates the G-CSF-mediated HSC repopulating defect. These data suggest that low level TLR agonist production by commensal flora contributes to the regulation of HSC function and that G-CSF negatively regulates HSCs, in part, by enhancing TLR signaling. RNA from KSL SLAM cells (Lineage- c-Kit+ Sca-1+ CD150+ CD48- CD41-) from bone marrow of 5-10 mice per group treated with G-CSF or saline alone was prepared using the RNA XS column kit (Machery-Nagel), amplified using the NuGen Ovation system (NuGen) and hybridized to the MoGene 1.0 ST array. This array includes 3 independent PBS control and 3 G-CSF treated groups.
2014-02-19 | E-GEOD-55094 | biostudies-arrayexpress
Project description:Recent studies demonstrate that inflammatory signals regulate hematopoietic stem cells (HSCs). Granulocyte-colony stimulating factor (G-CSF) is often induced with infection and plays a key role in the stress granulopoiesis response. However, its effects on HSCs are less clear. Herein, we show that treatment with G-CSF induces expansion and increased quiescence of phenotypic HSCs, but causes a marked, cell-autonomous HSC repopulating defect associated with induction of toll-like receptor (TLR) expression and signaling. The G-CSF-mediated expansion of HSCs is reduced in mice lacking TLR2, TLR4 or the TLR signaling adaptor MyD88. Induction of HSC quiescence is abrogated in mice lacking MyD88 or in mice treated with antibiotics to suppress intestinal flora. Finally, loss of TLR4 or germ free conditions mitigates the G-CSF-mediated HSC repopulating defect. These data suggest that low level TLR agonist production by commensal flora contributes to the regulation of HSC function and that G-CSF negatively regulates HSCs, in part, by enhancing TLR signaling. RNA from KSL SLAM cells (Lineage- c-Kit+ Sca-1+ CD150+ CD48- CD41-) from bone marrow of 5-10 mice per group treated with G-CSF or saline alone was prepared using the RNA XS column kit (Machery-Nagel), amplified using the NuGen Ovation system (NuGen) and hybridized to the MoGene 1.0 ST array. This array includes 4 independent PBS control and 4 G-CSF treated groups.
2014-02-19 | E-GEOD-55093 | biostudies-arrayexpress
Project description:The human intestine is colonized with a complex microbial community and forms a super organism with the human body. Intestinal microorganisms include more than 1,000 kinds of bacterias, and their flora is very complex and functions are very diverse. The intestinal flora affects the body’s nutrition, immunity and metabolism through interaction with the human body and the external environment, and is closely related to multiple systems. When the flora structure and function are changed, it will lead to the occurrence of various diseases or increase the risk of disease. In recent years, the role of intestinal microbes in tumorigenesis and development, as well as the role of diagnosis and treatment have been paid more and more attention. Abnormal intestinal flora can not only promote tumorigenesis, but also affect radiochemotherapy and immunotherapy effects. It is worth noting that the huge impact of the intestinal flora on immunotherapy suggests that immune checkpoint inhibitors can maximize the efficacy by protecting the balance and diversity of the intestinal microecology. Therefore, in this study, quantitative analysis of the diversity and abundance of intestinal, urinary tract flora, and urine components before and after adjuvant chemotherapy in patients with gastric and bowel cancer was performed. The link between treatment efficacy and prognosis.
| 2324613 | ecrin-mdr-crc