Impact of ROS-Induced Damage of TCA Cycle Enzymes on Metabolism and Virulence of Salmonella enterica serovar Typhimurium

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dc.contributor.authorNoster, Janina
dc.contributor.authorPersicke, Marcus
dc.contributor.authorChao, Tzu-Chiao
dc.contributor.authorKrone, Lena
dc.contributor.authorHeppner, Bianca
dc.contributor.authorHensel, Michael
dc.contributor.authorHansmeier, Nicole
dc.date.accessioned2023-05-23T19:10:01Z
dc.date.available2023-05-23T19:10:01Z
dc.date.issued2019-04-24
dc.description© 2019 Noster, Persicke, Chao, Krone, Heppner, Hensel and Hansmeier. 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.en_US
dc.description.abstractSalmonella enterica serovar Typhimurium (STM) is exposed to reactive oxygen species (ROS) originating from aerobic respiration, antibiotic treatment, and the oxidative burst occurring inside the Salmonella-containing vacuole (SCV) within host cells. ROS damage cellular compounds, thereby impairing bacterial viability and inducing cell death. Proteins containing iron–sulfur (Fe–S) clusters are particularly sensitive and become non-functional upon oxidation. Comprising five enzymes with Fe–S clusters, the TCA cycle is a pathway most sensitive toward ROS. To test the impact of ROS-mediated metabolic perturbations on bacterial physiology, we analyzed the proteomic and metabolic profile of STM deficient in both cytosolic superoxide dismutases (ΔsodAB). Incapable of detoxifying superoxide anions (SOA), endogenously generated SOA accumulate during growth. ΔsodAB showed reduced abundance of aconitases, leading to a metabolic profile similar to that of an aconitase-deficient strain (ΔacnAB). Furthermore, we determined a decreased expression of acnA in STM ΔsodAB. While intracellular proliferation in RAW264.7 macrophages and survival of methyl viologen treatment were not reduced for STM ΔacnAB, proteomic profiling revealed enhanced stress response. We conclude that ROS-mediated reduced expression and damage of aconitase does not impair bacterial viability or virulence, but might increase ROS amounts in STM, which reinforces the bactericidal effects of antibiotic treatment and immune responses of the host.en_US
dc.description.authorstatusFacultyen_US
dc.description.peerreviewyesen_US
dc.description.sponsorshipThis work was supported by the DFG by grant P15 within SFB 944, and HE1964/14-2 within priority program SPP1316.en_US
dc.identifier.citationNoster J, Persicke M, Chao T-C, Krone L, Heppner B, Hensel M and Hansmeier N (2019) Impact of ROS-Induced Damage of TCA Cycle Enzymes on Metabolism and Virulence of Salmonella enterica serovar Typhimurium. Front. Microbiol. 10:762. doi: 10.3389/fmicb.2019.00762en_US
dc.identifier.doihttps://doi.org/10.3389/fmicb.2019.00762
dc.identifier.urihttps://hdl.handle.net/10294/15931
dc.language.isoenen_US
dc.publisherFrontiers Mediaen_US
dc.rightsAttribution 4.0 United States*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.titleImpact of ROS-Induced Damage of TCA Cycle Enzymes on Metabolism and Virulence of Salmonella enterica serovar Typhimuriumen_US
dc.typeArticleen_US
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