Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress

Summary: Phagocytic leukocytes employ reactive oxygen species to defend against pathogenic microorganisms. The bacterial pathogen Staphylococcus aureus adapts to oxidative stress by producing antioxidant enzymes and small molecules to protect proteins, nucleic acids, and other essential cellular com...

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Main Authors: Iván C. Acosta, Andrew Albers, Liwei Fang, Gustavo Serrato, Wei Ping Teoh, David G. Glanville, Francis Alonzo, III
Format: Article
Language:English
Published: Elsevier 2025-08-01
Series:Cell Reports
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Online Access:http://www.sciencedirect.com/science/article/pii/S2211124725008666
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author Iván C. Acosta
Andrew Albers
Liwei Fang
Gustavo Serrato
Wei Ping Teoh
David G. Glanville
Francis Alonzo, III
author_facet Iván C. Acosta
Andrew Albers
Liwei Fang
Gustavo Serrato
Wei Ping Teoh
David G. Glanville
Francis Alonzo, III
author_sort Iván C. Acosta
collection DOAJ
description Summary: Phagocytic leukocytes employ reactive oxygen species to defend against pathogenic microorganisms. The bacterial pathogen Staphylococcus aureus adapts to oxidative stress by producing antioxidant enzymes and small molecules to protect proteins, nucleic acids, and other essential cellular components. Here, we show that the lipoic acid carrier protein GcvH-L promotes S. aureus resistance to oxidative stress. The gene encoding GcvH-L lies within a conserved operon in several pathogenic microorganisms. The operon also encodes LplA2, a redox-responsive lipoyl ligase, and SirTM, an ADP-ribosyltransferase. We demonstrate that ADP-ribosylation of lipoyl-GcvH-L protects lipoic acid from oxidation and regulates its transfer from GcvH-L to enzyme complexes needed for central metabolism. A ΔgcvH-L mutant is attenuated during infection and is more sensitive to phagocyte respiratory burst, phenotypes that are abrogated in NADPH oxidase-deficient mice. Thus, ADP-ribosylation and lipoylation converge on GcvH-L to promote S. aureus resistance to oxidative stress.
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spelling doaj-art-83ce02c721074338aeb5ea00ee61c12d2025-08-20T03:32:58ZengElsevierCell Reports2211-12472025-08-0144811609510.1016/j.celrep.2025.116095Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stressIván C. Acosta0Andrew Albers1Liwei Fang2Gustavo Serrato3Wei Ping Teoh4David G. Glanville5Francis Alonzo, III6Department of Microbiology and Immunology, University of Illinois at Chicago – College of Medicine, Chicago, IL, USADepartment of Microbiology and Immunology, University of Illinois at Chicago – College of Medicine, Chicago, IL, USADepartment of Microbiology and Immunology, University of Illinois at Chicago – College of Medicine, Chicago, IL, USADepartment of Microbiology and Immunology, University of Illinois at Chicago – College of Medicine, Chicago, IL, USA; Department of Microbiology and Immunology, Loyola University Chicago – Stritch School of Medicine, Maywood, IL, USADepartment of Microbiology and Immunology, Loyola University Chicago – Stritch School of Medicine, Maywood, IL, USADepartment of Microbiology and Immunology, Loyola University Chicago – Stritch School of Medicine, Maywood, IL, USADepartment of Microbiology and Immunology, University of Illinois at Chicago – College of Medicine, Chicago, IL, USA; Corresponding authorSummary: Phagocytic leukocytes employ reactive oxygen species to defend against pathogenic microorganisms. The bacterial pathogen Staphylococcus aureus adapts to oxidative stress by producing antioxidant enzymes and small molecules to protect proteins, nucleic acids, and other essential cellular components. Here, we show that the lipoic acid carrier protein GcvH-L promotes S. aureus resistance to oxidative stress. The gene encoding GcvH-L lies within a conserved operon in several pathogenic microorganisms. The operon also encodes LplA2, a redox-responsive lipoyl ligase, and SirTM, an ADP-ribosyltransferase. We demonstrate that ADP-ribosylation of lipoyl-GcvH-L protects lipoic acid from oxidation and regulates its transfer from GcvH-L to enzyme complexes needed for central metabolism. A ΔgcvH-L mutant is attenuated during infection and is more sensitive to phagocyte respiratory burst, phenotypes that are abrogated in NADPH oxidase-deficient mice. Thus, ADP-ribosylation and lipoylation converge on GcvH-L to promote S. aureus resistance to oxidative stress.http://www.sciencedirect.com/science/article/pii/S2211124725008666CP: MicrobiologyCP: Molecular biology
spellingShingle Iván C. Acosta
Andrew Albers
Liwei Fang
Gustavo Serrato
Wei Ping Teoh
David G. Glanville
Francis Alonzo, III
Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress
Cell Reports
CP: Microbiology
CP: Molecular biology
title Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress
title_full Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress
title_fullStr Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress
title_full_unstemmed Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress
title_short Staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress
title_sort staphylococcus aureus exploits lipoic acid salvage to combat host oxidative stress
topic CP: Microbiology
CP: Molecular biology
url http://www.sciencedirect.com/science/article/pii/S2211124725008666
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AT liweifang staphylococcusaureusexploitslipoicacidsalvagetocombathostoxidativestress
AT gustavoserrato staphylococcusaureusexploitslipoicacidsalvagetocombathostoxidativestress
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