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Interferon-γ response against C. burnetii of peripheral blood mononuclear cells in the development of chronic Q fever

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE66476 | GEO | 2016/03/13

SECONDARY ACCESSION(S): PRJNA277039

REPOSITORIES: GEO

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Interferon-Î³ response against C. burnetii of peripheral blood mononuclear cells in the development of chronic Q fever

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-Î³ response in chronic Q fever patients. Methods: IFN-Î³ was measured in supernatants of C. burnetii-stimulated peripheral blood mononuclear cells (PBMCs) of patients. Gene-expression profiles of the IFN-Î³ pathway in PBMCs after incubation with C. burnetii were compared between chronic Q fever patients and control individuals. Results: IFN-Î³ 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-Î³ were strongly upregulated in patients. Conclusion: Present study showed that IFN-Î³ production and the response to IFN-Î³ 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

Granulomatous response to Coxiella burnetii, the agent of Q fever: Activation of type I interferon-related genes

Project description:The formation of granulomas is associated with the resolution of Q fever, a zoonosis due to Coxiella burnetii; however the molecular mechanisms of granuloma formation remain poorly understood. We generated human granulomas with peripheral blood mononuclear cells and beads coated with C. burnetii, using BCG extracts as controls. A microarray analysis showed dramatic changes in gene expression in granuloma cells compared with peripheral blood mononuclear cells. About 60% of modulated genes were common to C. burnetii and BCG granulomas including M1-related genes. C. burnetii granulomas also expressed a specific transcriptional profile that was essentially enriched in genes associated with type I interferon response (IFI44, IFI44L, IFI6, OAS1, OAS2, OAS3, ISG15, IFIT1, IFITM2, IFITM3, MX1 and MX2). Real-time RT-PCR confirmed that C. burnetii especially increased the expression of interferon-stimulated genes in granulomas generated from controls or Q fever patients. Our results showed that granuloma formation is associated with a core of transcriptional response, but that the granulomatous response to C. burnetii is characterized by the activation of type I interferon-related genes, conferring a new role for type I interferon response in the control of C. burnetii infection. Human Peripheral Blood Mononuclear Cells (PBMC) were co-cultured with beads coated with Mycobacterium bovis strain Bacille Calmette Guerin (BCG) extracts or Coxiella burnetii (C.burnetii) extracts for 8 days and PBMC at day 0 were used as controls. For each condition ( unstimulated, BCG and C.burnetii), each microarray is a replicate of the same biological sample.

2015-05-01 | E-GEOD-37666 | biostudies-arrayexpress

Granulomatous response to Coxiella burnetii, the agent of Q fever: Activation of type I interferon-related genes

2015-05-01 | GSE37666 | GEO

Transcription profiling of human monocytes and monocyte-derived macrophages infected with Coxiella burnetii and incubated with apoptotic or necrotic lymphocytes

Project description:Q fever is due to Coxiella burnetii, an obligate intracellular bacterium. We investigated the mechanism of establishment of chronic form of the Q fever that mainlym anifested by endocarditis. We showed that patients with acute Q fever and valvulopathy, who have the higher risk to develop an endocarditis, exhibited high levels of circulating apoptotic cells. We further investigated the effect of the uptake of dead cells on the intracellular fate of the bacterium and the immune response of monocytes and macrophages.

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Coxiella burnetii infects JEG trophoblastic cell line, a model of placenta infection

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

Coxiella burnetii, the agent of Q fever, persists in adipocytes

2014-05-25 | GSE46335 | GEO

Coxiella burnetii, the agent of Q fever, persists in adipocytes

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

Host cell-free growth of the Q fever bacterium Coxiella burnetii

Project description:The inability to propagate obligate intracellular pathogens under axenic (host cell-free) culture conditions imposes severe experimental constraints that have negatively impacted progress in understanding pathogen virulence and disease mechanisms. Coxiella burnetii, the causative agent of human Q (Query) fever, is an obligate intracellular bacterial pathogen that replicates exclusively in an acidified, lysosome-like vacuole. To define conditions that support C. burnetii growth, we systematically evaluated the organismâ??s metabolic requirements using expression microarrays, genomic reconstruction, and metabolite typing. This led to development of a complex nutrient medium that supported substantial growth (~ 3 log10) of C. burnetii in a 2.5% oxygen environment. Importantly, axenically grown C. burnetii were highly infectious for Vero cells and exhibited developmental forms characteristic of in vivo grown organisms. Axenic cultivation of C. burnetii will facilitate studies of the organismâ??s pathogenesis and genetics, and aid development of Q fever preventatives such as an effective subunit vaccine. Furthermore, the systematic approach used here may be broadly applicable to development of axenic media that support growth of other medically important obligate intracellular pathogens. Host cell-free growth, Vero cell growth and carryover baseline of Coxiella burnetii

2010-06-20 | E-GEOD-13338 | biostudies-arrayexpress

Early response of Coxiella burnetii to temperature stress

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

Coxiella burnetii infects JEG trophoblastic cell line, a model of placenta infection

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