Signal-mediated interactions between Pseudomonas aeruginosa and Candida albicans

Abstract

Pseudomonas aeruginosa causes infections in a wide variety of hosts and is the leading cause of mortality in cystic fibrosis (CF) patients. Although most clinical isolates of P. aeruginosa share common virulence determinants, it is known that strains evolve and change phenotypically during CF lung infections. These changes can include alterations in the levels of N-acyl homoserine lactones (HSLs), which are secreted signal molecules. In the CF lung, fungi, especially Candida albicans and Aspergillus fumigatus, may coexist with P. aeruginosa but the implications for disease are not known. Recent studies have established that signalling can occur between P. aeruginosa and C. albicans, with the bacterial molecule 3-oxo-C12HSL affecting Candida morphology, and the fungal metabolite farnesol reducing levels of the Pseudomonas quinolone signal and pyocyanin in Pseudomonas. Whether these interactions are common and typical in clinical strains of P. aeruginosa was addressed using CF isolates that produced varied levels of HSLs. It was found that, whereas some clinical P. aeruginosa strains affected C. albicans morphology, others did not. This correlated closely with the amounts of 3-oxo-C12HSL produced by the isolates. Furthermore, it was established that signalling is bidirectional and that the C. albicans molecule farnesol inhibits swarming motility in P. aeruginosa CF strains. This work demonstrates that clinical isolates of these opportunistic pathogens can interact in strain-specific ways via secreted signals and illustrates the importance of studying these interactions to fully understand the microbial contribution to disease in polymicrobial infections.

The Multiple Signaling Systems Regulating Virulence in Pseudomonas aeruginosa

“…These two organisms share ecological niches, and both produce signals capable of interfering with the production of virulence factors by the other. Production of 3-oxo-C 12 -HSL by P. aeruginosa inhibits C. albicans filamentation, a crucial virulence adaptation for the development of opportunistic infections (90), while production of the fungal metabolite farnesol reduces PQS and pyocyanin levels and swarming motility in P. aeruginosa (39,132). The slight structural resemblance (C 12 FIG 6 PVD signaling pathway in P. aeruginosa.…”

Outcome and Prevention of Pseudomonas aeruginosa-Staphylococcus aureus Interactions During Pulmonary Infections in Cystic Fibrosis

“…Accordingly, and as previously underlined, infections of the CF airways is highly polymicrobic and there is growing evidence that many of these microorganisms interact (Sibley & Surette, 2011) as observed between P. aeruginosa and S. aureus (Biswas et al, 2009;Hoffman et al, 2006;Mitchell et al, 2010b;Qazi et al, 2006;Yang et al, 2011), P. aeruginosa and Burkholderia spp. (Bakkal et al, 2010;Chattoraj et al, 2010;Riedel et al, 2001;Weaver & Kolter, 2004), P. aeruginosa and S. maltophilia , P. aeruginosa and C. albicans (McAlester et al, 2008), and more generally with a large proportion of the organisms found in the CF airways (Duan et al, 2003;Sibley et al, 2008).…”

Cross-feeding and interkingdom communication in dual-species biofilms of Streptococcus mutans and Candida albicans

“…Hyphae development in C. albicans can be inhibited by 3-oxo-C12-homoserine lactone from Pseudomonas aeruginosa (Hogan et al, 2004), the S. mutans pheromone CSP (competence-stimulating peptide) (Jarosz et al, 2009) or by the diffusible signal factor trans-2-decenoic acid (Vilchez et al, 2010). Conversely, the signalling molecule farnesol from C. albicans inhibits the swarming motility of P. aeruginosa (McAlester et al, 2008) and induces the Pseudomonas quinolone signal synthesis (Cugini et al, 2010). No report exists of the induction of the quorum sensing signalling circuit of an oral pathogen by a eukaryotic fungus.…”