Interactions between Pseudomonas aeruginosa and Staphylococcus aureus during co-cultivations and polymicrobial infections

Nguyen, Angela T.; Oglesby-Sherrouse, Amanda G.

doi:10.1007/s00253-016-7596-3

Cited by 92 publications

(84 citation statements)

References 75 publications

(100 reference statements)

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“…[1] The opportunistic human pathogens Pseudomonas aeruginosa and Staphylococcus aureus are both capable of causing ab road variety of diseases,ranging from simple skin infections to lifethreatening sepsis and endocarditis.B oth species are frequently involved in polymicrobial infections where they engage in ab road range of interactions with major impact on the development and progression of infectious diseases. [2] Most frequently,h owever, the interactions of P. aeruginosa and S. aureus have been described as being of competitive nature. [3] Cystic fibrosis patients are initially colonized prevalently by S. aureus,w hich in later stages is largely replaced by P. aeruginosa although neither species completely disappears during any stage of the chronic disease.…”

mentioning

confidence: 99%

An Unsaturated Quinolone N‐Oxide of Pseudomonas aeruginosa Modulates Growth and Virulence of Staphylococcus aureus

Szamosvári

Böttcher

2017

Angew Chem Int Ed

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The pathogen Pseudomonas aeruginosa produces over 50 different quinolones, 16 of which belong to the class of 2-alkyl-4-quinolone N-oxides (AQNOs) with various chain lengths and degrees of saturation. We present the first synthesis of a previously proposed unsaturated compound that is confirmed to be present in culture extracts of P. aeruginosa, and its structure is shown to be trans-Δ -2-(non-1-enyl)-4-quinolone N-oxide. This compound is the most active agent against S. aureus, including MRSA strains, by more than one order of magnitude whereas its cis isomer is inactive. At lower concentrations, the compound induces small-colony variants of S. aureus, reduces the virulence by inhibiting hemolysis, and inhibits nitrate reductase activity under anaerobic conditions. These studies suggest that this unsaturated AQNO is one of the major agents that are used by P. aeruginosa to modulate competing bacterial species.

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mentioning

confidence: 99%

An Unsaturated Quinolone N‐Oxide of Pseudomonas aeruginosa Modulates Growth and Virulence of Staphylococcus aureus

Szamosvári

Böttcher

2017

Angew Chem Int Ed

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“…P. aeruginosa and S. aureus coexist within the CF lung, where a heterogeneous array of microorganisms, the host immune system, and nutrient availability all contribute to a complex and dynamic environment (8, 13, 31). Here we demonstrate that alginate, which is known to impact both host-pathogen and pathogen-pathogen interactions, also indirectly impacts pathogen-pathogen interactions (51, 52).…”

Section: Discussionmentioning

confidence: 99%

“…Studies of P. aeruginosa - S. aureus interactions have demonstrated that P. aeruginosa kills S. aureus in vitro , and this interaction is thought to contribute to the dominance of P. aeruginosa over S. aureus as CF patients age (30, 31). Considerable progress has been made in elucidating the mechanism of S. aureus killing mediated by P. aeruginosa (32–35).…”

Section: Introductionmentioning

confidence: 99%

Exogenous alginate protectsStaphylococcus aureusfrom killing byPseudomonas aeruginosa

Price¹,

Brown

Limoli

et al. 2019

Preprint

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Cystic fibrosis (CF) patients chronically infected with both Pseudomonas aeruginosa 22 with both P. aeruginosa and S. aureus have worse outcomes than mono-infected patients, and 44 both species persist within the same physical space in the lungs of CF patients. A variety of host 45 and environmental factors have been demonstrated to promote P. aeruginosa-S. aureus co-46 existence, despite evidence that P. aeruginosa kills S. aureus when these organisms are co-47 cultured in vitro. Thus, a better understanding of P. aeruginosa-S. aureus interactions, 48 particularly mechanisms by which these microorganisms are able to co-exist in proximal 49 physical space, will lead to better informed treatments for chronic polymicrobial infections. 50 51 have markedly improved patient survival (2,(16)(17)(18)(19), but despite these recent advances, the 60 progression of CF pulmonary disease is one of chronic infection and inflammation punctuated 61 by periods of clinical exacerbation which cause irreversible damage to lung tissue (2, 8,(20)(21)(22). 62Pseudomonas aeruginosa and Staphylococcus aureus are the two opportunistic 63 pathogens most commonly isolated from CF patients' lungs (2), and co-infection with both 64 microbes is common (23, 24). Co-infection with P. aeruginosa and S. aureus alters antibiotic 65 tolerance (25-28) and enhances virulence (29) in chronic infection. Furthermore, CF patients 66 who are co-infected with both P. aeruginosa and S. aureus have poorer clinical outcomes than 67 those who are mono-infected (23). 68Studies of P. aeruginosa-S. aureus interactions have demonstrated that P. aeruginosa 69 kills S. aureus in vitro, and this interaction is thought to contribute to the dominance of P. 70 aeruginosa over S. aureus as CF patients age (30, 31). Considerable progress has been made in 71 elucidating the mechanism of S. aureus killing mediated by P. aeruginosa (32)(33)(34)(35). P. aeruginosa 72 secretes quorum sensing regulated antimicrobial exoproducts during acute infection, including 73 2-heptyl-4-hydroxyquinoline N-oxide (HQNO), siderophores, rhamnolipids, and phenazines. 74 HQNO and the two P. aeruginosa siderophores, pyoverdine and pyochelin, have been shown to 75 drive S. aureus towards a fermentative lifestyle (33), while rhamnolipids disrupt cell membrane 76 integrity (33, 36). Phenazines inhibit S. aureus metabolism, as well as play a role in iron 77 acquisition and biofilm development (37-39). 78Chronic CF infection is marked by the emergence of mucoid P. aeruginosa isolates, 79 which overproduce the exopolysaccharide alginate (40, 41). P. aeruginosa virulence towards S. 80 aureus is decreased due to the overproduction of alginate, which causes transcriptional 81 downregulation of HQNO, siderophores, and rhamnolipids (32, 33, 42). The mechanism of 82 alginate overproduction is typically due to mutation in the mucA gene (43-45), a negative 83 regulator of  22 (AlgT/U) (43, 44, 46). De-repression of  22 promotes transcription of many 84 genes, but disruption of algD, the first gene in the algi...

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“…Die für den Menschen fakultativ pathogenen Bakterien Pseudomonas aeruginosa und Staphylococcus aureus sind beide in der Lage, eine Vielzahl an Krankheiten zu verursachen, die von einfachen Hautinfektionen bis hin zu lebensbedrohlicher Sepsis oder Endokarditis reichen. Beide Spezies sind häufig an polymikrobiellen Infektionen beteiligt, wobei sie durch ihre gegenseitigen Wechselwirkungen einen entscheidenden Einfluss auf die Entwicklung und den Verlauf von infektiösen Krankheiten nehmen . Am häufigsten wurden die Wechselwirkungen zwischen P. aeruginosa und S. aureus allerdings als kompetitiv beschrieben .…”

Section: Figureunclassified

Ein ungesättigtes Chinolon‐N‐oxid von Pseudomonas aeruginosa moduliert Wachstum und Virulenz von Staphylococcus aureus

Szamosvári

Böttcher

2017

Angewandte Chemie

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Das Humanpathogen Pseudomonas aeruginosa produziert über 50 verschiedene Chinolone,von denen 16 zur Klasse der 2-Alkyl-4-chinolon-N-oxide (AQNOs) gehçren, die in Länge und Sättigung der Seitenkette variieren. Wirberichten hier über die erste Synthese einer zuvor vermuteten ungesättigten AQNO-Variante,d ie wir in Kulturextrakten von P. aeruginosa bestätigen und deren Struktur als trans-D 1 -2-(Non-1-enyl)-4-chinolon-N-oxid aufklären konnten. Während das cis-Isomer inaktiv ist, zeigt die trans-Verbindung Aktivität gegen S. aureus,e inschließlich MRSA, die um mehr als eine Grçßenordnung hçher ist als die der übrigen AQNOs.B ei niedrigen Konzentrationen induziert die Verbindung das Wachstum kleiner Kolonievarianten von S. aureus und inhibiert dessen Virulenz durch Hemmung der Hämolyse sowie unter anaeroben Bedingungen die Aktivitätd er Nitratreduktase.U nsere Untersuchungen lassen vermuten, dass das ungesättigte AQNO einer der Hauptwirkstoffe von P. aeruginosa ist, durch den es konkurrierende Bakterienspezies moduliert.

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Interactions between Pseudomonas aeruginosa and Staphylococcus aureus during co-cultivations and polymicrobial infections

Cited by 92 publications

References 75 publications

An Unsaturated Quinolone N‐Oxide of Pseudomonas aeruginosa Modulates Growth and Virulence of Staphylococcus aureus

An Unsaturated Quinolone N‐Oxide of Pseudomonas aeruginosa Modulates Growth and Virulence of Staphylococcus aureus

Exogenous alginate protectsStaphylococcus aureusfrom killing byPseudomonas aeruginosa

Ein ungesättigtes Chinolon‐N‐oxid von Pseudomonas aeruginosa moduliert Wachstum und Virulenz von Staphylococcus aureus

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