Mus musculus
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ABSTRACT:
PROVIDER: PRJNA126755 | ENA |
REPOSITORIES: ENA
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Project description:Q fever, a zoonosis due to Coxiella burnetii infection, exhibits sexual dimorphism; men are affected more frequently and severely than women for a given exposure. Here we explore whether the severity of C. burnetii infection in mice is related to differences in male and female gene expression profiles. Mice were infected with C. burnetii for 24 hours, and gene expression was measured in liver cells using microarrays. Multiclass analysis identified 2,777 probes for which expression was specifically modulated by C. burnetti infection. Only 14% of the modulated genes were sex-independent, and the remaining 86% were differentially expressed in males and females. Castration of males and females showed that sex hormones were responsible for more than 60% of the observed gene modulation, and this reduction was most pronounced in males. Using functional annotation of modulated genes, we identified four clusters enriched in males that were related to cell-cell adhesion, signal transduction, defensins and cytokine/Jak-Stat pathways. Up-regulation of the IL-10 and Stat-3 genes may account for the high susceptibility of men with Q fever to C. burnetii infection and autoantibody production. Two clusters were identified in females, including the circadian rhythm pathway, which consists of positive (Clock, Arntl) and negative (Per) limbs of a feedback loop. We found that Clock and Arntl were down-modulated whereas Per was up-regulated; these changes may be associated with efficient bacterial elimination in females but not in males, in which an exacerbated host response would be prominent. This large-scale study revealed for the first time that circadian rhythm plays a major role in the anti-infectious response of mice, and it provides a new basis for elucidating the role of sexual dimorphism in human infections. Liver transcriptome was analyzed using whole genome microarray. Forty mice were divided into 8 groups of five mice upon three binary factors: sex, infection and castration. Four Samples were excluded from final analysis (see Data Processing for additional details).
2010-10-02 | E-GEOD-21065 | biostudies-arrayexpress
Project description:Q fever, a zoonosis due to Coxiella burnetii infection, exhibits sexual dimorphism; men are affected more frequently and severely than women for a given exposure. Here we explore whether the severity of C. burnetii infection in mice is related to differences in male and female gene expression profiles. Mice were infected with C. burnetii for 24 hours, and gene expression was measured in liver cells using microarrays. Multiclass analysis identified 2,777 probes for which expression was specifically modulated by C. burnetti infection. Only 14% of the modulated genes were sex-independent, and the remaining 86% were differentially expressed in males and females. Castration of males and females showed that sex hormones were responsible for more than 60% of the observed gene modulation, and this reduction was most pronounced in males. Using functional annotation of modulated genes, we identified four clusters enriched in males that were related to cell-cell adhesion, signal transduction, defensins and cytokine/Jak-Stat pathways. Up-regulation of the IL-10 and Stat-3 genes may account for the high susceptibility of men with Q fever to C. burnetii infection and autoantibody production. Two clusters were identified in females, including the circadian rhythm pathway, which consists of positive (Clock, Arntl) and negative (Per) limbs of a feedback loop. We found that Clock and Arntl were down-modulated whereas Per was up-regulated; these changes may be associated with efficient bacterial elimination in females but not in males, in which an exacerbated host response would be prominent. This large-scale study revealed for the first time that circadian rhythm plays a major role in the anti-infectious response of mice, and it provides a new basis for elucidating the role of sexual dimorphism in human infections.
2010-10-02 | GSE21065 | 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: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
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:Genotyping based on genomic comparative hybridization of different isolates of coxiella burnetii compared to NMI reference strain
2011-12-31 | GSE31543 | GEO
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.
2015-05-01 | GSE37666 | 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. Four experiments : Cold shock 30 min Vs 35°C; Cold shock 60 min Vs 35°C; Heat shock 30 min Vs 35°C; Heat shock 60 min Vs 35°C 3 biological replicates, independently grown and harvested. Four replicate per array.
2011-01-01 | E-GEOD-21778 | 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. 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: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