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Pseudomonas aeruginosa produces aspirin insensitive eicosanoids and contributes to the eicosanoid profile of polymicrobial biofilms with Candida albicans
Abstract The interaction of clinically relevant microorganisms is the focus of various studies, e.g. the interaction between the pathogenic yeast, Candida albicans , and the bacterium, Pseudomonas aeruginosa . During infection both release arachidonic acid, which they can transform into eicosanoids....
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Published in: | Prostaglandins, leukotrienes and essential fatty acids leukotrienes and essential fatty acids, 2017-02, Vol.117, p.36-46 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Abstract The interaction of clinically relevant microorganisms is the focus of various studies, e.g. the interaction between the pathogenic yeast, Candida albicans , and the bacterium, Pseudomonas aeruginosa . During infection both release arachidonic acid, which they can transform into eicosanoids. This study evaluated the production of prostaglandin E2 , prostaglandin F2α and 15-hydroxyeicosatetraenoic acid by biofilms of P. aeruginosa and C. albicans. The influence of co-incubation, acetylsalicylic acid and nordihydroguaiaretic acid on biofilm formation and eicosanoid production was evaluated. Acetylsalicylic acid decreased colony forming units of P. aeruginosa , but increased metabolic activity and eicosanoid production of the cells. In contrast to prostaglandin E2 , prostaglandin F2a production by C. albicans was insensitive to acetylsalicylic acid, indicating that different enzymes are responsible for their production in this yeast. Nordihydroguaiaretic acid inhibited biofilm formation by P. aeruginosa , however co-incubation provided protection against this inhibitor. Production of these eicosanoids could affect pathogen-clearance and infection dynamics and this previously uncharacterized facet of interaction could facilitate novel therapeutic intervention against polymicrobial infection. |
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ISSN: | 0952-3278 1532-2823 |
DOI: | 10.1016/j.plefa.2017.01.008 |