Selective Inhibition of Coxiella burnetii Replication by the Steroid Hormone Progesterone

  title={Selective Inhibition of Coxiella burnetii Replication by the Steroid Hormone Progesterone},
  author={Zachary P. Howard and Anders Omsland},
  journal={Infection and Immunity},
Coxiella burnetii is a zoonotic bacterial obligate intracellular parasite and the cause of query (Q) fever. During natural infection of female animals, C. burnetii shows tropism for the placenta and is associated with late-term abortion, at which time the pathogen titer in placental tissue can exceed one billion bacteria per gram. During later stages of pregnancy, placental trophoblasts serve as the major source of progesterone, a steroid hormone known to affect the replication of some… 
Impact of Sex Hormones on Macrophage Responses to Coxiella burnetii
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Metabolic Plasticity Aids Amphotropism of Coxiella burnetii
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Multispecies Q Fever Outbreak in a Mixed Dairy Goat and Cattle Farm Based on a New Bovine-Associated Genotype of Coxiella burnetii
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Gene-Specific Sex Effects on Susceptibility to Infectious Diseases
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Effect of sex on Coxiella burnetii infection: protective role of 17beta-estradiol.
Results show that sex hormones control host response to C. burnetii infection and may account for host-dependent clinical presentation of Q fever.
Q Fever in Pregnant Goats: Pathogenesis and Excretion of Coxiella burnetii
These results are the first to demonstrate that pregnant goats can be infected via the intranasal route with a recent Dutch outbreak of C. burnetii, an intracellular bacterial pathogen that causes Q fever and has a strong tropism for the trophoblasts of the placenta and is not excreted before parturition.
From Q Fever to Coxiella burnetii Infection: a Paradigm Change
All the progress made over the last 20 years on this topic are reviewed, including the breaking of the old dichotomy between “acute” and “chronic” Q fever and the achievement of determining the genome sequences of several strains of this species and comparative genomic analyses.
Host cell-free growth of the Q fever bacterium Coxiella burnetii
Axenic cultivation of C. burnetii will facilitate studies of the organism's pathogenesis and genetics and aid development of Q fever preventatives such as an effective subunit vaccine and may be broadly applicable to development of axenic media that support growth of other medically important obligate intracellular pathogens.
Use of Axenic Culture Tools to Study Coxiella burnetii
In this unit, the media currently utilized for axenic culture of C. burnetii are described and, to aid in experimental reproducibility and interpretation of results, considerations and limitations are discussed.
Complete genome sequence of the Q-fever pathogen Coxiella burnetii
Analysis of the genome of Coxiella burnetii, Nine Mile phase I RSA493, a highly virulent zoonotic pathogen and category B bioterrorism agent, was sequenced by the random shotgun method, suggesting that the obligate intracellular lifestyle of C. burningetii may be a relatively recent innovation.
Effect of Progesterone on Neisseria gonorrhoeae
The effects of progesterone on the growth of pathogenic and nonpathogenic species of Neisseria were studied in liquid cultures. Only strains of N. gonorrhoeae and N. meningitidis were highly
Natural history and pathophysiology of Q fever.
Coxiella burnetii Isolates Cause Genogroup-Specific Virulence in Mouse and Guinea Pig Models of Acute Q Fever
Isolates from all of the groups produced disease in the SCID mouse model, and genogroup-consistent trends were noted in cytokine production in response to infection in the immunocompetent-mouse model.
Coxiella burnetii Phase I and II Variants Replicate with Similar Kinetics in Degradative Phagolysosome-Like Compartments of Human Macrophages
Infection of primary human monocyte-derived macrophages and THP-1 cells as host cells is employed to directly compare the PV maturation kinetics and pathogen growth in cells infected with the Nine Mile phase I variant (NMI) or phase II variant (NMII) of C. burnetii, suggesting that C. burningetii does not actively inhibit phagolysosome function as a survival mechanism.