Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> Infection
<i>Staphylococcus aureus</i> is a metabolically flexible pathogen that causes infection in diverse settings. An array of virulence factors, including the secreted toxins, enables <i>S. aureus</i> to colonize different environmental niches and initiate infections by any of sev...
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-09-01
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| Series: | Toxins |
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| Online Access: | https://www.mdpi.com/2072-6651/12/9/581 |
| _version_ | 1797554174804623360 |
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| author | Tania Wong Fok Lung Alice Prince |
| author_facet | Tania Wong Fok Lung Alice Prince |
| author_sort | Tania Wong Fok Lung |
| collection | DOAJ |
| description | <i>Staphylococcus aureus</i> is a metabolically flexible pathogen that causes infection in diverse settings. An array of virulence factors, including the secreted toxins, enables <i>S. aureus</i> to colonize different environmental niches and initiate infections by any of several discrete pathways. During these infections, both <i>S. aureus</i> and host cells compete with each other for nutrients and remodel their metabolism for survival. This metabolic interaction/crosstalk determines the outcome of the infection. The reprogramming of metabolic pathways in host immune cells not only generates adenosine triphosphate (ATP) to meet the cellular energy requirements during the infection process but also activates antimicrobial responses for eventual bacterial clearance, including cell death pathways. The selective pressure exerted by host immune cells leads to the emergence of bacterial mutants adapted for chronicity. These host-adapted mutants are often characterized by substantial changes in the expression of their own metabolic genes, or by mutations in genes involved in metabolism and biofilm formation. Host-adapted <i>S. aureus</i> can rewire or benefit from the metabolic activities of the immune cells via several mechanisms to cause persistent infection. In this review, we discuss how <i>S. aureus</i> activates host innate immune signaling, which results in an immune metabolic pressure that shapes <i>S. aureus</i> metabolic adaptation and determines the outcome of the infection. |
| first_indexed | 2024-03-10T16:26:58Z |
| format | Article |
| id | doaj.art-eea43677c5b3463d86539f305863682c |
| institution | Directory Open Access Journal |
| issn | 2072-6651 |
| language | English |
| last_indexed | 2024-03-10T16:26:58Z |
| publishDate | 2020-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Toxins |
| spelling | doaj.art-eea43677c5b3463d86539f305863682c2023-11-20T13:09:11ZengMDPI AGToxins2072-66512020-09-0112958110.3390/toxins12090581Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> InfectionTania Wong Fok Lung0Alice Prince1Department of Pediatrics, Vagelos College of Physicians & Surgeons, Columbia University, New York, NY 10032, USADepartment of Pediatrics, Vagelos College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA<i>Staphylococcus aureus</i> is a metabolically flexible pathogen that causes infection in diverse settings. An array of virulence factors, including the secreted toxins, enables <i>S. aureus</i> to colonize different environmental niches and initiate infections by any of several discrete pathways. During these infections, both <i>S. aureus</i> and host cells compete with each other for nutrients and remodel their metabolism for survival. This metabolic interaction/crosstalk determines the outcome of the infection. The reprogramming of metabolic pathways in host immune cells not only generates adenosine triphosphate (ATP) to meet the cellular energy requirements during the infection process but also activates antimicrobial responses for eventual bacterial clearance, including cell death pathways. The selective pressure exerted by host immune cells leads to the emergence of bacterial mutants adapted for chronicity. These host-adapted mutants are often characterized by substantial changes in the expression of their own metabolic genes, or by mutations in genes involved in metabolism and biofilm formation. Host-adapted <i>S. aureus</i> can rewire or benefit from the metabolic activities of the immune cells via several mechanisms to cause persistent infection. In this review, we discuss how <i>S. aureus</i> activates host innate immune signaling, which results in an immune metabolic pressure that shapes <i>S. aureus</i> metabolic adaptation and determines the outcome of the infection.https://www.mdpi.com/2072-6651/12/9/581<i>Staphylococcus aureus</i>small colony variants (SCVs)biofilmmetabolic adaptationmetabolic reprogrammingcell death |
| spellingShingle | Tania Wong Fok Lung Alice Prince Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> Infection Toxins <i>Staphylococcus aureus</i> small colony variants (SCVs) biofilm metabolic adaptation metabolic reprogramming cell death |
| title | Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> Infection |
| title_full | Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> Infection |
| title_fullStr | Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> Infection |
| title_full_unstemmed | Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> Infection |
| title_short | Consequences of Metabolic Interactions during <i>Staphylococcus aureus</i> Infection |
| title_sort | consequences of metabolic interactions during i staphylococcus aureus i infection |
| topic | <i>Staphylococcus aureus</i> small colony variants (SCVs) biofilm metabolic adaptation metabolic reprogramming cell death |
| url | https://www.mdpi.com/2072-6651/12/9/581 |
| work_keys_str_mv | AT taniawongfoklung consequencesofmetabolicinteractionsduringistaphylococcusaureusiinfection AT aliceprince consequencesofmetabolicinteractionsduringistaphylococcusaureusiinfection |