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Recent Advances on the Innate Immune Response to Coxiella burnetii

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...

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Autores principales: Sireci, Guido, Badami, Giusto Davide, Di Liberto, Diana, Blanda, Valeria, Grippi, Francesca, Di Paola, Laura, Guercio, Annalisa, de la Fuente, José, Torina, Alessandra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8593175/
https://www.ncbi.nlm.nih.gov/pubmed/34796128
http://dx.doi.org/10.3389/fcimb.2021.754455
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author Sireci, Guido
Badami, Giusto Davide
Di Liberto, Diana
Blanda, Valeria
Grippi, Francesca
Di Paola, Laura
Guercio, Annalisa
de la Fuente, José
Torina, Alessandra
author_facet Sireci, Guido
Badami, Giusto Davide
Di Liberto, Diana
Blanda, Valeria
Grippi, Francesca
Di Paola, Laura
Guercio, Annalisa
de la Fuente, José
Torina, Alessandra
author_sort Sireci, Guido
collection PubMed
description 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.
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spelling pubmed-85931752021-11-17 Recent Advances on the Innate Immune Response to Coxiella burnetii Sireci, Guido Badami, Giusto Davide Di Liberto, Diana Blanda, Valeria Grippi, Francesca Di Paola, Laura Guercio, Annalisa de la Fuente, José Torina, Alessandra Front Cell Infect Microbiol Cellular and Infection Microbiology 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. Frontiers Media S.A. 2021-11-02 /pmc/articles/PMC8593175/ /pubmed/34796128 http://dx.doi.org/10.3389/fcimb.2021.754455 Text en Copyright © 2021 Sireci, Badami, Di Liberto, Blanda, Grippi, Di Paola, Guercio, de la Fuente and Torina https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular and Infection Microbiology
Sireci, Guido
Badami, Giusto Davide
Di Liberto, Diana
Blanda, Valeria
Grippi, Francesca
Di Paola, Laura
Guercio, Annalisa
de la Fuente, José
Torina, Alessandra
Recent Advances on the Innate Immune Response to Coxiella burnetii
title Recent Advances on the Innate Immune Response to Coxiella burnetii
title_full Recent Advances on the Innate Immune Response to Coxiella burnetii
title_fullStr Recent Advances on the Innate Immune Response to Coxiella burnetii
title_full_unstemmed Recent Advances on the Innate Immune Response to Coxiella burnetii
title_short Recent Advances on the Innate Immune Response to Coxiella burnetii
title_sort recent advances on the innate immune response to coxiella burnetii
topic Cellular and Infection Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8593175/
https://www.ncbi.nlm.nih.gov/pubmed/34796128
http://dx.doi.org/10.3389/fcimb.2021.754455
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