Abstract
Coxiella burnetii is an obligate intracellular Gram-negative bacterium and the causative agent of a worldwide zoonosis known as Q fever. The pathogen invades monocytes and macrophages, replicating within acidic phagolysosomes and evading host defenses through different immune evasion strategies that are mainly associated with the structure of its lipopolysaccharide. The main transmission routes are aerosols and ingestion of fomites from infected animals. The innate immune system provides the first host defense against the microorganism, and it is crucial to direct the infection towards a self-limiting respiratory disease or the chronic form. This review reports the advances in understanding the mechanisms of innate immunity acting during C. burnetii infection and the strategies that pathogen put in place to infect the host cells and to modify the expression of specific host cell genes in order to subvert cellular processes. The mechanisms through which different cell types with different genetic backgrounds are differently susceptible to C. burnetii intracellular growth are discussed. The subsets of cytokines induced following C. burnetii infection as well as the pathogen influence on an inflammasome-mediated response are also described. Finally, we discuss the use of animal experimental systems for studying the innate immune response against C. burnetii and discovering novel methods for prevention and treatment of disease in humans and livestock.
Highlights
Coxiella burnetii is an obligate intracellular Gram-negative bacterium (Dragan and Voth, 2020) that can be transmitted by aerosol with a very low infectious dose, as 1–10 viable organisms are sufficient to induce in humans an infection via the aerogenic route (Moos and Hackstadt, 1987; Sawyer et al, 1987; Gürtler et al, 2014)
This review is focused on recent advances in the comprehension of innate immune mechanisms involved in protection against C. burnetii infection and the strategies elicited by the pathogen to invade the host cells and actively regulate the expression of specific host cell genes to subvert cellular processes
Coxiella burnetii showed a limited ability of alveolar macrophage activation, as it was supported by studies showing that the interactions between C. burnetii and the Ctype lectin surfactant protein D (SP-D), a member of the innate immune response in different mucosal surfaces and in the lungs, result in bacterial aggregation provoking pathogen killing and clearance
Summary
Guido Sireci 1, Giusto Davide Badami 1, Diana Di Liberto 1, Valeria Blanda 2*, Francesca Grippi 2, Laura Di Paola 2, Annalisa Guercio 2, Josede la Fuente 3,4 and Alessandra Torina 2. Specialty section: This article was submitted to Microbes and Innate Immunity, a section of the journal Frontiers in Cellular and Infection Microbiology. The innate immune system provides the first host defense against the microorganism, and it is crucial to direct the infection towards a self-limiting respiratory disease or the chronic form. This review reports the advances in understanding the mechanisms of innate immunity acting during C. burnetii infection and the strategies that pathogen put in place to infect the host cells and to modify the expression of specific host cell genes in order to subvert cellular processes. We discuss the use of animal experimental systems for studying the innate immune response against C. burnetii and discovering novel methods for prevention and treatment of disease in humans and livestock
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