Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species.
Staphylococcus aureus is a human commensal organism and opportunist pathogen, causing potentially fatal disease. The presence of non-pathogenic microflora or their components, at the point of infection, dramatically increases S. aureus pathogenicity, a process termed augmentation. Augmentation is as...
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2021
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oai:doaj.org-article:589ad2747e0c478eacd842d8f79203f32021-12-02T20:00:10ZCommensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species.1553-73661553-737410.1371/journal.ppat.1009880https://doaj.org/article/589ad2747e0c478eacd842d8f79203f32021-09-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.1009880https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Staphylococcus aureus is a human commensal organism and opportunist pathogen, causing potentially fatal disease. The presence of non-pathogenic microflora or their components, at the point of infection, dramatically increases S. aureus pathogenicity, a process termed augmentation. Augmentation is associated with macrophage interaction but by a hitherto unknown mechanism. Here, we demonstrate a breadth of cross-kingdom microorganisms can augment S. aureus disease and that pathogenesis of Enterococcus faecalis can also be augmented. Co-administration of augmenting material also forms an efficacious vaccine model for S. aureus. In vitro, augmenting material protects S. aureus directly from reactive oxygen species (ROS), which correlates with in vivo studies where augmentation restores full virulence to the ROS-susceptible, attenuated mutant katA ahpC. At the cellular level, augmentation increases bacterial survival within macrophages via amelioration of ROS, leading to proliferation and escape. We have defined the molecular basis for augmentation that represents an important aspect of the initiation of infection.Josie F GibsonGrace R PidwillOliver T CarnellBas G J SurewaardDaria ShamarinaJoshua A F SuttonCharlotte JefferyAurélie Derré-BobillotCristel ArchambaudMatthew K SigginsEric J G PollittSimon A JohnstonPascale SerrorShiranee SriskandanStephen A RenshawSimon J FosterPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 17, Iss 9, p e1009880 (2021) |
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DOAJ |
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DOAJ |
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| topic |
Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 |
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Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Josie F Gibson Grace R Pidwill Oliver T Carnell Bas G J Surewaard Daria Shamarina Joshua A F Sutton Charlotte Jeffery Aurélie Derré-Bobillot Cristel Archambaud Matthew K Siggins Eric J G Pollitt Simon A Johnston Pascale Serror Shiranee Sriskandan Stephen A Renshaw Simon J Foster Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species. |
| description |
Staphylococcus aureus is a human commensal organism and opportunist pathogen, causing potentially fatal disease. The presence of non-pathogenic microflora or their components, at the point of infection, dramatically increases S. aureus pathogenicity, a process termed augmentation. Augmentation is associated with macrophage interaction but by a hitherto unknown mechanism. Here, we demonstrate a breadth of cross-kingdom microorganisms can augment S. aureus disease and that pathogenesis of Enterococcus faecalis can also be augmented. Co-administration of augmenting material also forms an efficacious vaccine model for S. aureus. In vitro, augmenting material protects S. aureus directly from reactive oxygen species (ROS), which correlates with in vivo studies where augmentation restores full virulence to the ROS-susceptible, attenuated mutant katA ahpC. At the cellular level, augmentation increases bacterial survival within macrophages via amelioration of ROS, leading to proliferation and escape. We have defined the molecular basis for augmentation that represents an important aspect of the initiation of infection. |
| format |
article |
| author |
Josie F Gibson Grace R Pidwill Oliver T Carnell Bas G J Surewaard Daria Shamarina Joshua A F Sutton Charlotte Jeffery Aurélie Derré-Bobillot Cristel Archambaud Matthew K Siggins Eric J G Pollitt Simon A Johnston Pascale Serror Shiranee Sriskandan Stephen A Renshaw Simon J Foster |
| author_facet |
Josie F Gibson Grace R Pidwill Oliver T Carnell Bas G J Surewaard Daria Shamarina Joshua A F Sutton Charlotte Jeffery Aurélie Derré-Bobillot Cristel Archambaud Matthew K Siggins Eric J G Pollitt Simon A Johnston Pascale Serror Shiranee Sriskandan Stephen A Renshaw Simon J Foster |
| author_sort |
Josie F Gibson |
| title |
Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species. |
| title_short |
Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species. |
| title_full |
Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species. |
| title_fullStr |
Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species. |
| title_full_unstemmed |
Commensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species. |
| title_sort |
commensal bacteria augment staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species. |
| publisher |
Public Library of Science (PLoS) |
| publishDate |
2021 |
| url |
https://doaj.org/article/589ad2747e0c478eacd842d8f79203f3 |
| work_keys_str_mv |
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| _version_ |
1718375722207150080 |