Prostaglandin production during growth of Candida albicans biofilms

Abstract

Both biofilms and planktonic (suspended) cells of Candida albicans synthesized extracellular prostaglandin(s) during growth at 37 8C, but biofilm cells secreted significantly more prostaglandin(s) when production was determined on the basis of cell dry weight. Prostaglandin synthesis by both cell types was sensitive to the cyclooxygenase inhibitors aspirin, diclofenac and etodolac. A morphological mutant blocked in two signalling pathways (cph1/cph1 efg1/ efg1) produced prostaglandin levels similar to those of the parent strain, but formed yeast-only biofilms. These results suggest that prostaglandin production could be a significant virulence factor in biofilm-associated infections, although its role in C. albicans morphogenesis remains unclear.

Effect of Some Non steroidal Anti-Inflammatory Drugs on Growth, Adherence and Mature Biofilms of <i>Candida spp</i><i>.</i>

“…High doses leads to the direct damage of membranes similar to that shown by SEM images in our study. Pina-Vaz et al, [43] showed that ibuprofen at low concentration inhibit growth in a manner resembles that shown by lipophilic azoles by interfering with the metabolic pathways more than by direct damage to membranes. Also, The concentration of ibuprofen in urine of patients under the conventional standard systemic regimens reaches values above those shown to possess an antifungal activity, pointing to the potential usefulness of ibuprofen for urinary tract candidosis.…”

“…Alem and Douglas [43] attributed the antifungal and antibiofilm activity to the diclofenac-induced increase of the membrane permeability of the C. albicans biofilm cells which may be a result of the effect of diclofenac on the biosynthesis of fungal prostaglandins. Also, they demonstrated that biofilms of various C. albicans isolates and strains, grown in the presence of diclofenac, showed increased susceptibility to caspofungin.…”

“…As eicosanoids pathway was reported to show a vital role in controlling yeast-hyphal transition and biofilm. So, drugs targeting fungal prostaglandins pathways may show great effects on fungal colonization and infection [21]. In addition, some studies showed that Sodium Diclofenac affect C. albicans morphogenesis and biofilm formation.…”

“…They are also found to be produced by C. albicans cells but their role in fungal biology is unknown [20]. Erb-Downward and Noverr [21] suggested that prostaglandins can act as regulators for C. albicans virulence. As eicosanoids pathway was reported to show a vital role in controlling yeast-hyphal transition and biofilm.…”

Candida albicans Biofilms Produce More Secreted Aspartyl Protease than the Planktonic Cells

“…5,6) There is now ample data that hyphal phase cells predominate in late biofilms compared with the planktonic phase where minimal if any, hyphal growth is present. 7) Additionally, relatively recent findings indicate that biofilm phase C. albicans compared to planktonic counterparts manifest other phenotypic alterations that enhance their virulence, such as increased prostaglandin secretion rates, 8) and cell surface hydrophobicity, 9) and decreased ergosterol levels in plasma membrane 10) that incur a substantial resistance to azoles and polyene antifungals. Our current data indicate that increased Sap production is yet another mechanism by which these yeasts persist on host surfaces in addition to the expression of the foregoing virulence attributes.…”