Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus

Detalhes bibliográficos
Autor(a) principal: Silva, Liliana O.
Data de Publicação: 2018
Outros Autores: Nobre, Lígia S., Mil-Homens, Dalila, Fialho, Arsénio, Saraiva, Lígia M.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
Texto Completo: https://doi.org/10.1080/21505594.2017.1389829
Resumo: RICs are a family of bacterial proteins involved in the repair of iron centers containing proteins damaged by the antimicrobial reactive species liberated by the innate immune system of infected hosts. Staphylococcus aureus is a human pathogen with increasing antibiotic resistance that also contains a RIC-like protein. In this work, we show that the survival of S. aureus within macrophages decreases upon inactivation of ric, and that the viability was restored to levels similar to the wild-type strain by reintroduction of ric via in trans complementation. Importantly, in macrophages that do not produce reactive oxygen species, the lower survival of the ric mutant was no longer observed. In lung epithelial cells, the intracellular viability of the S. aureus ric mutant was also shown to be lower than that of the wild-type. The wax moth larvae Galleria mellonella infected with S. aureus ric mutant presented an approximately 2.5-times higher survival when compared to the wild-type strain. Moreover, significantly lower bacterial loads were determined in the larvae hemolymph infected with strains not expressing ric, and complementation assays confirmed that this behavior was related to RIC. Furthermore, expression of the S. aureus ric gene within the larvae increased along the course of infection with a ~20-fold increase after 8 h of infection. Altogether, the data show that RIC is important for the virulence of S. aureus.
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spelling Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureusdi-iron proteinGalleria mellonellainnate immunity Staphylococcus aureusParasitologyMicrobiologyImmunologyMicrobiology (medical)Infectious DiseasesSDG 3 - Good Health and Well-beingRICs are a family of bacterial proteins involved in the repair of iron centers containing proteins damaged by the antimicrobial reactive species liberated by the innate immune system of infected hosts. Staphylococcus aureus is a human pathogen with increasing antibiotic resistance that also contains a RIC-like protein. In this work, we show that the survival of S. aureus within macrophages decreases upon inactivation of ric, and that the viability was restored to levels similar to the wild-type strain by reintroduction of ric via in trans complementation. Importantly, in macrophages that do not produce reactive oxygen species, the lower survival of the ric mutant was no longer observed. In lung epithelial cells, the intracellular viability of the S. aureus ric mutant was also shown to be lower than that of the wild-type. The wax moth larvae Galleria mellonella infected with S. aureus ric mutant presented an approximately 2.5-times higher survival when compared to the wild-type strain. Moreover, significantly lower bacterial loads were determined in the larvae hemolymph infected with strains not expressing ric, and complementation assays confirmed that this behavior was related to RIC. Furthermore, expression of the S. aureus ric gene within the larvae increased along the course of infection with a ~20-fold increase after 8 h of infection. Altogether, the data show that RIC is important for the virulence of S. aureus.Molecular, Structural and Cellular Microbiology (MOSTMICRO)Instituto de Tecnologia Química e Biológica António Xavier (ITQB)Universidade NOVA de LisboaRUNSilva, Liliana O.Nobre, Lígia S.Mil-Homens, DalilaFialho, ArsénioSaraiva, Lígia M.2019-05-03T22:17:05Z2018-01-012018-01-01T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article6application/pdfhttps://doi.org/10.1080/21505594.2017.1389829eng2150-5594PURE: 13051339http://www.scopus.com/inward/record.url?scp=85037664838&partnerID=8YFLogxKhttps://doi.org/10.1080/21505594.2017.1389829info:eu-repo/semantics/openAccessreponame:Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)instname:FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiainstacron:RCAAP2024-05-22T17:39:13Zoai:run.unl.pt:10362/68568Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireinfo@rcaap.ptopendoar:https://opendoar.ac.uk/repository/71602025-05-28T17:10:12.815271Repositórios Científicos de Acesso Aberto de Portugal (RCAAP) - FCCN, serviços digitais da FCT – Fundação para a Ciência e a Tecnologiafalse
dc.title.none.fl_str_mv Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
title Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
spellingShingle Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
Silva, Liliana O.
di-iron protein
Galleria mellonella
innate immunity Staphylococcus aureus
Parasitology
Microbiology
Immunology
Microbiology (medical)
Infectious Diseases
SDG 3 - Good Health and Well-being
title_short Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
title_full Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
title_fullStr Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
title_full_unstemmed Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
title_sort Repair of Iron Centers RIC protein contributes to the virulence of Staphylococcus aureus
author Silva, Liliana O.
author_facet Silva, Liliana O.
Nobre, Lígia S.
Mil-Homens, Dalila
Fialho, Arsénio
Saraiva, Lígia M.
author_role author
author2 Nobre, Lígia S.
Mil-Homens, Dalila
Fialho, Arsénio
Saraiva, Lígia M.
author2_role author
author
author
author
dc.contributor.none.fl_str_mv Molecular, Structural and Cellular Microbiology (MOSTMICRO)
Instituto de Tecnologia Química e Biológica António Xavier (ITQB)
Universidade NOVA de Lisboa
RUN
dc.contributor.author.fl_str_mv Silva, Liliana O.
Nobre, Lígia S.
Mil-Homens, Dalila
Fialho, Arsénio
Saraiva, Lígia M.
dc.subject.por.fl_str_mv di-iron protein
Galleria mellonella
innate immunity Staphylococcus aureus
Parasitology
Microbiology
Immunology
Microbiology (medical)
Infectious Diseases
SDG 3 - Good Health and Well-being
topic di-iron protein
Galleria mellonella
innate immunity Staphylococcus aureus
Parasitology
Microbiology
Immunology
Microbiology (medical)
Infectious Diseases
SDG 3 - Good Health and Well-being
description RICs are a family of bacterial proteins involved in the repair of iron centers containing proteins damaged by the antimicrobial reactive species liberated by the innate immune system of infected hosts. Staphylococcus aureus is a human pathogen with increasing antibiotic resistance that also contains a RIC-like protein. In this work, we show that the survival of S. aureus within macrophages decreases upon inactivation of ric, and that the viability was restored to levels similar to the wild-type strain by reintroduction of ric via in trans complementation. Importantly, in macrophages that do not produce reactive oxygen species, the lower survival of the ric mutant was no longer observed. In lung epithelial cells, the intracellular viability of the S. aureus ric mutant was also shown to be lower than that of the wild-type. The wax moth larvae Galleria mellonella infected with S. aureus ric mutant presented an approximately 2.5-times higher survival when compared to the wild-type strain. Moreover, significantly lower bacterial loads were determined in the larvae hemolymph infected with strains not expressing ric, and complementation assays confirmed that this behavior was related to RIC. Furthermore, expression of the S. aureus ric gene within the larvae increased along the course of infection with a ~20-fold increase after 8 h of infection. Altogether, the data show that RIC is important for the virulence of S. aureus.
publishDate 2018
dc.date.none.fl_str_mv 2018-01-01
2018-01-01T00:00:00Z
2019-05-03T22:17:05Z
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dc.identifier.uri.fl_str_mv https://doi.org/10.1080/21505594.2017.1389829
url https://doi.org/10.1080/21505594.2017.1389829
dc.language.iso.fl_str_mv eng
language eng
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PURE: 13051339
http://www.scopus.com/inward/record.url?scp=85037664838&partnerID=8YFLogxK
https://doi.org/10.1080/21505594.2017.1389829
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