There are many examples of the interaction between prokaryotes and eukaryotes. One such example is the polymicrobial colonization/infection by the various opportunistic pathogenic yeasts belonging to the genus Candida and the ubiquitous bacterium, Pseudomonas aeruginosa. Although this interaction has simplistically been characterized as antagonistic to the yeast, this review highlights the complexity of the interaction with various factors influencing both microbes. The first section deals with the interactions in vitro, looking specifically at the role of cell wall components, quorum sensing molecules, phenazines, fatty acid metabolites and competition for iron in the interaction. The second part of this review places all these interactions in the context of various infection or colonization sites, i.e., lungs, wounds, and the gastrointestinal tract. Here we see that the role of the host, as well as the methodology used to establish co-infection, are important factors, influencing the outcome of the disease. Suggested future perspectives for the study of this interaction include determining the influence of newly identified participants of the QS network of P. aeruginosa, oxylipin production by both species, as well as the genetic and phenotypic plasticity of these microbes, on the interaction and outcome of co-infection.

Candida albicans is frequently co-isolated with the Gram-negative bacterium, Pseudomonas aeruginosa. In vitro, the interaction is complex, with both species influencing each other. Not only does the bacterium kill hyphal cells of C. albicans through physical interaction, it also affects C. albicans biofilm formation and morphogenesis, through various secreted factors and cell wall components. The present study sought to expand the current knowledge regarding the interaction between C. albicans and P. aeruginosa, using transcriptome analyses of early static biofilms. Under these conditions, a total of 2,537 open reading frames (approximately 40% of the C. albicans transcriptome) was differentially regulated in the presence of P. aeruginosa. Upon deeper analyses it became evident that the response of C. albicans toward P. aeruginosa was dominated by a response to hypoxia, and included those associated with stress as well as iron and zinc homeostasis. These conditions may also lead to the observed differential regulation of genes associated with cell membrane synthesis, morphology, biofilm formation and phenotypic switching. Thus, C. albicans in polymicrobial biofilms with P. aeruginosa have unique transcriptional profiles that may influence commensalism as well as pathogenesis.

Candida albicansis an opportunistic yeast pathogen within the human microbiota with significant medical importance because of its pathogenic potential. The yeast produces highly resistant biofilms, which are crucial for maintaining infections. Though antifungals are available, their effectiveness is dwindling due to resistance. Alternate options that comprise the combination of existing azoles and polyunsaturated fatty acids, such as arachidonic acid (AA), have been shown to increase azoles susceptibility ofC. albicansbiofilms; however, the mechanisms are still unknown. Therefore, transcriptome analysis was conducted on biofilms exposed to sub-inhibitory concentrations of AA alone, fluconazole alone, and AA combined with fluconazole to understand the possible mechanism involved with the phenomenon.ProteinANalysisTHroughEvolutionaryRelationships (PANTHER) analysis from the differentially expressed genes revealed that the combination of AA and fluconazole influences biological processes associated with essential processes including methionine synthesis and those involved in ATP generation, such as AMP biosynthesis, fumarate metabolism and fatty acid oxidation. These observations suggests that the interference of AA with these processes may be a possible mechanisms to induce increased antifungal susceptibility.

The nonpolar lipids present in cells are mainly triacylglycerols and steryl esters. When cells are provided with an abundance of nutrients, these storage lipids accumulate. As large quantities of nonpolar lipids cannot be integrated into membranes, they are isolated from the cytosolic environment in lipid droplets. As specialized, inducible cytoplasmic organelles, lipid droplets have functions beyond the regulation of lipid metabolism, in cell signalling and activation, membrane trafficking and control of inflammatory mediator synthesis and secretion. Pathogens, including fungi, viruses, parasites, or intracellular bacteria can induce and may benefit from lipid droplets in infected cells. Here we review biogenesis of lipid droplets as well as the role of lipid droplets in the pathogenesis of selected viruses, bacteria, protists and yeasts.