dc.contributor.author
Linzner, Nico
dc.contributor.author
Loi, Vu Van
dc.contributor.author
Antelmann, Haike
dc.date.accessioned
2022-10-20T14:23:45Z
dc.date.available
2022-10-20T14:23:45Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/36620
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-36333
dc.description.abstract
Staphylococcus aureus has to cope with oxidative stress during infections. In this study, S. aureus was found to be resistant to 100 mM H2O2 during aerobic growth. While KatA was essential for this high aerobic H2O2 resistance, the peroxiredoxin AhpC contributed to detoxification of 0.4 mM H2O2 in the absence of KatA. In addition, the peroxiredoxins AhpC, Tpx and Bcp were found to be required for detoxification of cumene hydroperoxide (CHP). The high H2O2 tolerance of aerobic S. aureus cells was associated with priming by endogenous H2O2 levels, which was supported by an oxidative shift of the bacillithiol redox potential to −291 mV compared to −310 mV in microaerophilic cells. In contrast, S. aureus could be primed by sub-lethal doses of 100 µM H2O2 during microaerophilic growth to acquire an improved resistance towards the otherwise lethal triggering stimulus of 10 mM H2O2. This microaerophilic priming was dependent on increased KatA activity, whereas aerobic cells showed constitutive high KatA activity. Thus, KatA contributes to the high H2O2 resistance of aerobic cells and to microaerophilic H2O2 priming in order to survive the subsequent lethal triggering doses of H2O2, allowing the adaptation of S. aureus under infections to different oxygen environments.
en
dc.format.extent
20 Seiten
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject
Staphylococcus aureus
en
dc.subject
H2O2 resistance
en
dc.subject.ddc
500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie::570 Biowissenschaften; Biologie
dc.title
The Catalase KatA Contributes to Microaerophilic H2O2 Priming to Acquire an Improved Oxidative Stress Resistance in Staphylococcus aureus
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
1793
dcterms.bibliographicCitation.doi
10.3390/antiox11091793
dcterms.bibliographicCitation.journaltitle
Antioxidants
dcterms.bibliographicCitation.number
9
dcterms.bibliographicCitation.originalpublishername
MDPI
dcterms.bibliographicCitation.volume
11
dcterms.bibliographicCitation.url
https://doi.org/10.3390/antiox11091793
refubium.affiliation
Biologie, Chemie, Pharmazie
refubium.affiliation.other
Institut für Biologie / Arbeitsbereich Mikrobiologie
refubium.note.author
Die Publikation wurde aus Open Access Publikationsgeldern der Freien Universität Berlin gefördert.
de
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.isPartOf.eissn
2076-3921