To die or not to die: Programmed cell death responses and their interactions with Coxiella burnetii infection.
To die or not to die: Programmed cell death responses and their interactions with Coxiella burnetii infection.
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DOI:
10.1111/mmi.14878
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发表时间:
2022-04
影响因子:
3.6
通讯作者:
Goodman, Alan G.
中科院分区:
文献类型:
--
作者:
Osbron, Chelsea A.;Goodman, Alan G.
Coxiella burnetii is a Gram-negative, obligate intracellular, macrophage-tropic bacterium and the causative agent of the zoonotic disease Q fever. The epidemiology of Q fever is associated with the presence of infected animals; sheep, goats, cattle, and humans primarily become infected by inhalation of contaminated aerosols. In humans, the acute phase of the disease is characterized primarily by influenza-like symptoms, and approximately 3–5% of the infected individuals develop chronic infection. C. burnetii infection activates many types of immune responses, and the bacteria’s genome encodes for numerous effector proteins that interact with host immune signaling mechanisms. Here, we will discuss two forms of programmed cell death, apoptosis and pyroptosis. Apoptosis is a form of non-inflammatory cell death that leads to phagocytosis of small membrane-bound bodies. Conversely, pyroptosis results in lytic cell death accompanied by the release of proinflammatory cytokines. Both apoptosis and pyroptosis have been implicated in the clearance of intracellular bacterial pathogens, including C. burnetii. Finally, we will discuss the role of autophagy, the degradation of unwanted cellular components, during C. burnetii infection. Together, the review of these forms of programmed cell death will open new research questions aimed at combating this highly infectious pathogen for which treatment options are limited. Coxiella burnetii is an obligate intracellular, macrophage-tropic bacterium and the causative agent of the zoonotic disease Q fever. In this review, we summarize the relationships between C. burnetii and the cellular processes of apoptosis, pyroptosis, and autophagy. Bacterial modulation of these pathways has been implicated in the maintenance of infection, and discussion of what is known regarding host-bacterial interactions will open new research questions aimed at understanding and combating this highly infectious pathogen.
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