The redox metabolic pathways function to limit Anaplasma phagocytophilum infection and multiplication while preserving fitness in tick vector cells
Autor: | Alberdi Vélez, María Pilar, Cabezas Cruz, Alejandro, Espinosa Prados, Pedro, Villar Rayo, Margarita María, Artigas Jerónimo, Sara, Fuente, José de la |
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Přispěvatelé: | SaBio, Instituto de Investigación en Recursos Cinegéticos (IREC), Biologie moléculaire et immunologie parasitaires et fongiques (BIPAR), École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA)-Laboratoire de santé animale, sites de Maisons-Alfort et de Dozulé, Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES)-Agence nationale de sécurité sanitaire de l'alimentation, de l'environnement et du travail (ANSES)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Department of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University [Stillwater], Research Plan of UCLM, Junta de Comunidades of Castilla-La Mancha (JCCM, Spain), Junta de Comunidades de Castilla-La Mancha, Universidad de Castilla La Mancha, Cabezas-Cruz, Alejandro [0000-0002-8660-730X], Espinosa, Pedro J. [0000-0003-2829-4779], Villar, Margarita [0000-0003-4172-9079], Fuente, José de la [0000-0001-7383-9649], École nationale vétérinaire - Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA)-Laboratoire de santé animale, sites de Maisons-Alfort et de Dozulé, Oklahoma State University [Stillwater] (OSU), Cabezas-Cruz, Alejandro, Espinosa, Pedro J., Villar, Margarita, Fuente, José de la |
Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
Anaplasmosis
Neutrophils [SDV]Life Sciences [q-bio] lcsh:Medicine HL-60 Cells Disease Vectors Article parasitic diseases Animals Humans Transcriptomics lcsh:Science Sheep Ixodes Mass spectrometry lcsh:R bacterial infections and mycoses Oxidative Stress Gene Expression Regulation Host-Pathogen Interactions lcsh:Q Rabbits Pathogens Infection Redox metabolic pathways Oxidation-Reduction Metabolic Networks and Pathways Anaplasma phagocytophilum Signal Transduction |
Zdroj: | Scientific Reports Scientific Reports, Nature Publishing Group, 2019, 9, ⟨10.1038/s41598-019-49766-x⟩ Scientific Reports, Vol 9, Iss 1, Pp 1-15 (2019) Digital.CSIC. Repositorio Institucional del CSIC instname |
ISSN: | 2045-2322 |
DOI: | 10.1038/s41598-019-49766-x⟩ |
Popis: | Aerobic organisms evolved conserved mechanisms controlling the generation of reactive oxygen species (ROS) to maintain redox homeostasis signaling and modulate signal transduction, gene expression and cellular functional responses under physiological conditions. The production of ROS by mitochondria is essential in the oxidative stress associated with different pathologies and in response to pathogen infection. Anaplasma phagocytophilum is an intracellular pathogen transmitted by Ixodes scapularis ticks and causing human granulocytic anaplasmosis. Bacteria multiply in vertebrate neutrophils and infect first tick midgut cells and subsequently hemocytes and salivary glands from where transmission occurs. Previous results demonstrated that A. phagocytophilum does not induce the production of ROS as part of its survival strategy in human neutrophils. However, little is known about the role of ROS during pathogen infection in ticks. In this study, the role of tick oxidative stress during A. phagocytophilum infection was characterized through the function of different pathways involved in ROS production. The results showed that tick cells increase mitochondrial ROS production to limit A. phagocytophilum infection, while pathogen inhibits alternative ROS production pathways and apoptosis to preserve cell fitness and facilitate infection. The inhibition of NADPH oxidase-mediated ROS production by pathogen infection appears to occur in both neutrophils and tick cells, thus supporting that A. phagocytophilum uses common mechanisms for infection of ticks and vertebrate hosts. However, differences in ROS response to A. phagocytophilum infection between human and tick cells may reflect host-specific cell tropism that evolved during pathogen life cycle. MV was supported by Research Plan of UCLM. PA was supported by the Junta de Comunidades of Castilla-La Mancha (JCCM, Spain). |
Databáze: | OpenAIRE |
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