Disease relevance of Coxiella

• These two polypeptides show homology with Escherichia coli groE and Coxiella burnetii htp heat-shock proteins [1].
• Monocytic THP-1 cells were infected with Coxiella burnetii, the etiological agent of Q fever, and then treated with IFN-gamma [2].
• Analysis of the TMD of DjlA and recently identified homologues in Coxiella burnetti and Haemophilus influenzae revealed a striking pattern of conserved glycines (or rarely alanine), with a four-residue spacing [3].
• The Coxiella dotB, icmS and icmW products restored dot/icm-dependent growth of Legionella mutants in eukaryotic host cells [4].
• Correlation between serum doxycycline concentrations and serologic evolution in patients with Coxiella burnetii endocarditis [5].

High impact information on Coxiella

• Stimulation of toll-like receptor 2 by Coxiella burnetii is required for macrophage production of pro-inflammatory cytokines and resistance to infection [6].
• IFN-gamma-induced apoptosis and microbicidal activity in monocytes harboring the intracellular bacterium Coxiella burnetii require membrane TNF and homotypic cell adherence [7].
• IFN-gamma-mediated control of Coxiella burnetii survival in monocytes: the role of cell apoptosis and TNF [2].
• Subversion of monocyte functions by coxiella burnetii: impairment of the cross-talk between alphavbeta3 integrin and CR3 [8].
• The degree of increase in proliferation induced by indomethacin correlated strongly with the amount of PGE2 produced in a 4-hr culture stimulated by Coxiella antigen, but it also correlated with the sensitivity to inhibition of mitogenesis by PGE2 [9].

Chemical compound and disease context of Coxiella

• Endotoxicosis induced by Coxiella burnetii lipopolysaccharide stimulates a ribosomal protein S6 kinase: some properties of the partially purified enzyme [10].
• Vaccines prepared from Formalin-killed whole cells of Coxiella burnetii (Ohio strain) or from chloroform-methanol residue (CMR) and extract (CME) of such cells were examined for biological and immunological properties in male C57BL/10ScN endotoxin nonresponder mice [11].
• BALB/cJ (H-2d) mice were injected intraperitoneally (ip) with cyclophosphamide 2 days after ip inoculation with Coxiella burnetii Nine Mile, phase I [12].
• Bactericidal effect of doxycycline associated with lysosomotropic agents on Coxiella burnetii in P388D1 cells [13].
• In vitro susceptibilities of spotted fever group rickettsiae and Coxiella burnetti to clarithromycin [14].

Biological context of Coxiella

• Comparative virulence of intra- and interstrain lipopolysaccharide variants of Coxiella burnetii in the guinea pig model [15].
• Antigenic variation in the phase I lipopolysaccharide of Coxiella burnetii isolates [16].
• Q fever, as well as the lipopolysaccharide prepared from the rickettsial agent Coxiella burnetii, stimulates the phosphorylation of guinea pig liver ribosomal protein S6 [17].
• Macrophage infectivity potentiator (CbMip, 23.5 kDa) protein of the obligate intracellular bacterium, Coxiella burnetii, was shown previously to belong to the family of FKBPs based on sequence homology and peptidyl-prolyl cis/trans isomerase (PPIase) activity [18].
• A Coxiella burnetii chromosomal fragment capable of functioning as an origin for the replication of a kanamycin resistance (Kanr) plasmid was isolated by use of origin search methods utilizing an Escherichia coli host [19].

Anatomical context of Coxiella

• High-speed supernatant fluids derived from sonicated Coxiella burnetii contained considerable acid phosphatase activity when assayed by using 4-methylumbelliferylphosphate; they also contained a factor that blocked superoxide anion production by human neutrophils stimulated with formyl-Met-Leu-Phe [20].
• Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages [21].
• Furthermore, 3-methyladenine and wortmannin, agents known to inhibit early stages in the autophagic process, each blocked Coxiella vacuole formation [22].
• Interferon-gamma inhibits growth of Coxiella burnetii in mouse fibroblasts [23].
• Inoculation with viable, but not inactivated, Coxiella burnetii resulted in the increased expression of transferrin receptors (TfR) in the murine macrophage-like cell line J774A [24].

Gene context of Coxiella

• Both inducible nitric oxide synthase and NADPH oxidase contribute to the control of virulent phase I Coxiella burnetii infections [25].
• This study examined the effect of nitric oxide produced by inducible nitric oxide synthase (iNOS) up-regulated in response to cytokine stimulation, or by a synthetic nitric oxide donor, on replication of obligately intracellular Coxiella burnetii in murine L-929 cells [26].
• Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever [27].
• Characterization of the Coxiella burnetti sucB gene encoding an immunogenic dihydrolipoamide succinyltransferase [28].
• Coxiella burnetii infection increases transferrin receptors on J774A. 1 cells [24].

Analytical, diagnostic and therapeutic context of Coxiella

• The DNA from the Nine Mile phase I strain of Coxiella burnetti, the etiological agent of Q fever, has been isolated and purified by cesium chloride-ethidium bromide density gradient centrifugation [29].
• A Coxiella burnetii Hsp70 homologue was identified by using an acid activation in vitro system in which protein synthesis has been followed by [35S]methionine labeling, autoradiography, and immunoblotting [30].
• Evaluation of a competitive enzyme immunoassay for detection of Coxiella burnetii antibody in animal sera [31].
• Molecular cloning of a Coxiella burnetii gene encoding a macrophage infectivity potentiator (Mip) analogue [32].
• The detection of Coxiella burnetii from ovine genital swabs, milk and fecal samples by the use of a single touchdown polymerase chain reaction [33].

References