Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA143619 | ENA |
REPOSITORIES: ENA
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Project description:Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium usually found in myeloid cells. The infection is a source of severe obstetrical complications in humans and cattle, and of chronic evolution in pregnant women. As C. burnetii is found in the placenta of aborted foetuses in humans and ruminants, we wondered if it may infect trophoblasts. In this work, we showed that C. burnetii, infected JEG trophoblastic cells without replication and was localized within phagolysosomes. We analyzed gene expression programs induced by C. burnetii in JEG trophoblastic cell line and compared it with transcriptomic program of BeWo trophoblasts in which C. burnetii replicates. These transcriptomic programs induced by C. burnetii in JEG trophoblasts was poor and markedly different from that induced by C. burnetii in BeWo trophoblasts. Hence, the differences in transcriptomic programs may explain the different intracellular fate of C. burnetii in JEG and BeWo cells. Our results suggest that C. burnetii may use trophoblastic cells as a reservoir by interfering with gene expression. Comparaison between unstimulated JEG cell line and Coxiella burnetii stimulated JEG cell line (bacterial ratio 200:1) for 6 hours
2012-12-07 | E-GEOD-30330 | biostudies-arrayexpress
Project description:Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium usually found in myeloid cells. The infection is a source of severe obstetrical complications in humans and cattle, and of chronic evolution in pregnant women. As C. burnetii is found in the placenta of aborted foetuses in humans and ruminants, we wondered if it may infect trophoblasts. In this work, we showed that C. burnetii, infected JEG trophoblastic cells without replication and was localized within phagolysosomes. We analyzed gene expression programs induced by C. burnetii in JEG trophoblastic cell line and compared it with transcriptomic program of BeWo trophoblasts in which C. burnetii replicates. These transcriptomic programs induced by C. burnetii in JEG trophoblasts was poor and markedly different from that induced by C. burnetii in BeWo trophoblasts. Hence, the differences in transcriptomic programs may explain the different intracellular fate of C. burnetii in JEG and BeWo cells. Our results suggest that C. burnetii may use trophoblastic cells as a reservoir by interfering with gene expression.
2012-12-07 | GSE30330 | GEO
Project description:Background: Q fever is caused by the Coxiella burnetii, an intracellular bacterium that infects mononuclear cells. In some individuals, it causes a persistent cardiovascular infection (chronic Q fever). The aim of present study was to investigate the C. burnetii-induced IFN-γ response in chronic Q fever patients. Methods: IFN-γ was measured in supernatants of C. burnetii-stimulated peripheral blood mononuclear cells (PBMCs) of patients. Gene-expression profiles of the IFN-γ pathway in PBMCs after incubation with C. burnetii were compared between chronic Q fever patients and control individuals. Results: IFN-γ production by PBMCs of chronic Q fever patients incubated with C. burnetii in vitro, was significantly higher compared to controls. In transcriptome analysis, genes downstream of IFN-γ were strongly upregulated in patients. Conclusion: Present study showed that IFN-γ production and the response to IFN-γ seems to be intact in chronic Q fever patients. PBMC were purified from Q fever patients (n=6) or healthy volunteers (n=4), and then stimulated by Coxiella burnetii, LPS or left untreated (NS)
2016-03-13 | E-GEOD-66476 | biostudies-arrayexpress
Project description:Two trophoblastic cell lines, CRL-1584 (3A-Sub E) and JEG-3 were purchased from American Type Culture collection (ATCC) (Manassas, VA). CRL-1584 (3A-Sub E) was originally derived from human term primary placental cells and then immortalized using SV40 virus. JEG-3 is a clonal human choriocarcinoma. The cell lines were serially passaged in complete medium supplemented with each cell lineâs respective IC50 concentration of methotrexate until the cell lines were able to proliferate normally. Subsequently, the concentration of methotrexate was increased by one half-log concentration. The process was repeated iteratively until the cells became senescent. At each log concentration of methotrexate resistance, cell line stocks were frozen to establish a separate subline of each cell line. Based on their relative level of resistance to methotrexate, these were designated JEG-3-R7, JEG-3-R6, and JEG-3-R5 (for 10-7 M through 10-5 M methotrexate resistance). Over the same time period (approximately 11 months), we were able to induce only one order of magnitude of resistance in the normal placenta cell line; that line was designated NP-R7. In parallel, the parent cell lines were passaged in normal medium to control for any physiologic changes induced by prolonged culture in vitro.
2017-10-17 | E-MTAB-5185 | biostudies-arrayexpress
Project description:Background: Q fever is caused by the Coxiella burnetii, an intracellular bacterium that infects mononuclear cells. In some individuals, it causes a persistent cardiovascular infection (chronic Q fever). The aim of present study was to investigate the C. burnetii-induced IFN-γ response in chronic Q fever patients. Methods: IFN-γ was measured in supernatants of C. burnetii-stimulated peripheral blood mononuclear cells (PBMCs) of patients. Gene-expression profiles of the IFN-γ pathway in PBMCs after incubation with C. burnetii were compared between chronic Q fever patients and control individuals. Results: IFN-γ production by PBMCs of chronic Q fever patients incubated with C. burnetii in vitro, was significantly higher compared to controls. In transcriptome analysis, genes downstream of IFN-γ were strongly upregulated in patients. Conclusion: Present study showed that IFN-γ production and the response to IFN-γ seems to be intact in chronic Q fever patients.
2016-03-13 | GSE66476 | GEO
Project description:Transcriptional profiling of Coxiella burnetii phase I (RSA 493) submitting either to Cold and Heat shock comparing to control untreated Coxiella burnetii phase I (RSA 493) grown at 35°C.
2011-01-01 | GSE21778 | GEO
Project description:Coxiella burnetii, the agent of Q fever, persists in humans despite specific immune responses: however, its reservoir remains unknown. We detected C. burnetii in adipose tissue from BALB/c and C57/BL6 mice 4 months after infection when no bacteria were found in other tissues. C. burnetii infected cultivated adipocytes, replicated within late phagosomes and induced a transcriptional program that was enriched for the expression of genes associated with inflammatory response, hormonal responses and cytoskeleton. 3T3-L1 (ATCC) differentiated adipocytes were stimulated or not with Coxiella burnetii (NMI) at a ratio of 50 bacteria per cell. Four biological replicates were analyzed in each group. Due to technical reason, one unstimulated sample was discarded from the analysis.
2014-05-25 | E-GEOD-46335 | biostudies-arrayexpress
Project description:Coxiella burnetii, the agent of Q fever, persists in humans despite specific immune responses: however, its reservoir remains unknown. We detected C. burnetii in adipose tissue from BALB/c and C57/BL6 mice 4 months after infection when no bacteria were found in other tissues. C. burnetii infected cultivated adipocytes, replicated within late phagosomes and induced a transcriptional program that was enriched for the expression of genes associated with inflammatory response, hormonal responses and cytoskeleton.
2014-05-25 | GSE46335 | GEO
Project description:Coxiella burnetii, the agent causing Q fever, has been associated with B-cell non-Hodgkin lymphoma (NHL). To better clarify this link, we analysed the genetic transcriptomic profile of peripheral blood leukocytes from patients with C. burnetii infection to identify possible links to lymphoma. Microarray analyses revealed that 1189 genes were expressed differently (p <.001 and fold change ≥4) in whole blood of patients with C. burnetii infection compared to controls. In addition, 95 genes expressed in patients with non-Hodgkin lymphoma (NHL) and in patients with C. burnetii persistent infection have allowed us to establish the ‘C. burnetii-associated NHL signature’. Among these, 33 genes previously found modulated in C. burnetii-associated -NHL by the microarray analysis were selected and their mRNA expression levels were measured in distinct C. burnetii-induced pathologies, namely, acute Q fever, focalized persistent infection, lymphadenitis and C.burnetii-associated NHL. Specific genes involved in anti-apoptotic process were found highly expressed in leukocytes from patients with C. burnetii associated-NHL: MIR17HG, REL and SP100. This signature differed from that found for NHL-control group. Patients with C. burnetii lymphadenitis presented significant elevated levels of BCL2 and ETS1 mRNAs. Altogether, we identified a specific transcriptionnal signature for NHL during C. burnetii infection reflecting the up-regulation of anti-apoptotic processes and the fact that lymphadenitis might constitute a critical step towards lymphomagenesis.
2019-06-05 | GSE112086 | GEO
Project description:A comparison was made between the THP-1(Human monocytic leukemia cells - TIB-202; ATCC) transcriptional responses of; (i) uninfected versus Coxiella burnetii NMII infected and (ii) uninfected versus Coxiella burnetii NMII infected THP-1 cells transiently treated with bacteriostatic levels (10μg/ml) of chloramphenicol (CAM). Briefly, infections were initiated and cultured in parallel with uninfected cells. At 48 hours post infection (hpi), media containing CAM (10μg/ml) was added to one set of cells (uninfected and infected THP-1 cells) and culturing was continued. The other set of cells were mock treated with normal media. Total RNA was isolated at 72 hpi from all conditions. Microarrays were performed for both condition sets and the results from each of the two microarrays were compared to define the host genes modulated by de novo C. burnetii NMII protein synthesis.
2010-10-01 | GSE23665 | GEO