scholarly journals Adaptive immunity to the obligate intracellular pathogen Coxiella burnetii

2008 ◽  
Vol 43 (1-3) ◽  
pp. 138-148 ◽  
Author(s):  
Jeffrey G. Shannon ◽  
Robert A. Heinzen
Keyword(s):  
Adaptive Immunity ◽  
Coxiella Burnetii ◽  
Intracellular Pathogen ◽  
Obligate Intracellular ◽  
Obligate Intracellular Pathogen

scholarly journals Coxiella burnetii Inhibits Activation of Host Cell Apoptosis through a Mechanism That Involves Preventing Cytochrome c Release from Mitochondria

2007 ◽  
Vol 75 (11) ◽  
pp. 5282-5289 ◽  
Author(s):  
Anja Lührmann ◽  
Craig R. Roy
Keyword(s):  
Cell Death ◽  
Host Cell ◽  
Coxiella Burnetii ◽  
Mammalian Cells ◽  
Q Fever ◽  
Host Cells ◽  
Intracellular Pathogen ◽  
Obligate Intracellular ◽  
Cell Death Pathway ◽  
Obligate Intracellular Pathogen

ABSTRACT Coxiella burnetii is an obligate intracellular pathogen and the etiological agent of the human disease Q fever. C. burnetii infects mammalian cells and then remodels the membrane-bound compartment in which it resides into a unique lysosome-derived organelle that supports bacterial multiplication. To gain insight into the mechanisms by which C. burnetii is able to multiply intracellularly, we examined the ability of host cells to respond to signals that normally induce apoptosis. Our data show that mammalian cells infected with C. burnetii are resistant to apoptosis induced by staurosporine and UV light. C. burnetii infection prevented caspase 3/7 activation and limited fragmentation of the host cell nucleus in response to agonists that induce apoptosis. Inhibition of bacterial protein synthesis reduced the antiapoptotic effect that C. burnetii exerted on infected host cells. Inhibition of apoptosis in C. burnetii-infected cells did not correlate with the degradation of proapoptotic BH3-only proteins involved in activation of the intrinsic cell death pathway; however, cytochrome c release from mitochondria was diminished in cells infected with C. burnetii upon induction of apoptosis. These data indicate that C. burnetii can interfere with the intrinsic cell death pathway during infection by producing proteins that either directly or indirectly prevent release of cytochrome c from mitochondria. It is likely that inhibition of apoptosis by C. burnetii represents an important virulence property that allows this obligate intracellular pathogen to maintain host cell viability despite inducing stress that would normally activate the intrinsic death pathway.

scholarly journals Seroprevalence of Coxiella burnetii in cattle in the Belgrade epizootiological area

2020 ◽  
Vol 36 (3) ◽  
pp. 359-369
Author(s):  
Jadranka Zutic ◽  
Dragica Vojinovic ◽  
Slobodan Stanojevic ◽  
Branislav Kureljusic ◽  
Vesna Milicevic ◽  
...  
Keyword(s):  
Coxiella Burnetii ◽  
Preventive Measures ◽  
Q Fever ◽  
Intracellular Pathogen ◽  
Reproductive Disorders ◽  
Serum Samples ◽  
Obligate Intracellular ◽  
Control Programs ◽  
Serological Studies ◽  
Obligate Intracellular Pathogen

Q-fever is antropozoonosis which is caused by Coxiella burnetii, obligate intracellular pathogen. The most significant characteristics of this pathogen are resistance and stability in the environment, possibility of aerosol dissemination, and very low infective dose. C. burnetii can infect domestic and wild animals, rodents, birds and ticks. Q fever in animals is generally asymptomatic, although it can lead to reproductive disorders during pregnancy. The main route of infection in humans is inhalation of contaminated aerosol and dust. Serological studies have shown the presence of antibodies to C. burnetii in the serum samples of cattle in Belgrade epizootiological area. Seroprevalence of 18% was found in farm bred cattle, while it was only 1.5% in individual breeding. In farm bred cows that have suffered abortion prevalence was 49%, and only 1.9% in individual breeding. The overall results indicate that the circulation of this pathogen in cattle, in Belgrade epizootiological area, poses a health risk, not only to the cattle, but also to the humans, especially persons working with animals. Q fever control programs most often recommend serological research and vaccination of animals. Accordingly, it is necessary to define a strategy for the implementation of biosecurity measures and preventive measures against Q fever.

Cell death and inflammation during infection with the obligate intracellular pathogen, Chlamydia

Biochimie ◽  
2003 ◽  
Vol 85 (8) ◽  
pp. 763-769 ◽  
Author(s):  
Jean-Luc Perfettini ◽  
Véronique Hospital ◽  
Lynn Stahl ◽  
Thomas Jungas ◽  
Philippe Verbeke ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracellular Pathogen ◽  
Obligate Intracellular ◽  
Obligate Intracellular Pathogen

scholarly journals Hijacking and Use of Host Kinases by Chlamydiae

Pathogens ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1034
Author(s):  
Prakash Sah ◽  
Erika I. Lutter
Keyword(s):  
Host Cell ◽  
Intracellular Pathogen ◽  
Host Proteins ◽  
Sexually Transmitted ◽  
Obligate Intracellular ◽  
Host Cell Apoptosis ◽  
Survival And Development ◽  
Causative Agents ◽  
Cell Processes ◽  
Obligate Intracellular Pathogen

Chlamydia species are causative agents of sexually transmitted infections, blinding trachoma, and animal infections with zoonotic potential. Being an obligate intracellular pathogen, Chlamydia relies on the host cell for its survival and development, subverting various host cell processes throughout the infection cycle. A key subset of host proteins utilized by Chlamydia include an assortment of host kinase signaling networks which are vital for many chlamydial processes including entry, nutrient acquisition, and suppression of host cell apoptosis. In this review, we summarize the recent advancements in our understanding of host kinase subversion by Chlamydia.

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