Inhibitory effect of cerulenin and sodium butyrate on germination of Candida albicans

Abstract

Candida albicans germination in liquid medium was inhibition by the antilipogenic agent cerulenin and the fatty acid sodium butyrate. Although these inhibitors prevented germ tube emergence at concentrations of 1 microgram/ml and 20 mM, respectively, neither significantly affected cell viability as judged by trypan blue staining or the rate of protein biosynthesis throughout the time course of the experiments. Cerulenin treatment resulted in inhibition of lipid biosynthesis, but lipid biosynthetic capabilities remained unaltered in sodium butyrate-supplemented cultures. Because each inhibitor blocks germination by different mechanisms, their utility in distinguishing events directly correlated to germination was examined. In this context, chitin synthase activity was inhibited by both compounds, confirming the importance of chitin biosynthesis in C. albicans germination.

Parenteral Lipid Emulsion Induces Germination ofCandida albicansand Increases Biofilm Formation on Medical Catheter Surfaces

“…Fatty acids contained in LE may play a role in C. albicans germination. For example, Hoberg et al [45] found that exposure to cerulenin, an antibiotic that inhibits fatty acid biosynthesis in yeast, inhibited germination in C. albicans through the inhibition of lipid biosynthesis. The addition of palmitic acid restored germination in cerulenin-inhibited cells.…”

A Pseudomonas aeruginosa quorum‐sensing molecule influences Candida albicans morphology

“…However, after treatment with broad‐spectrum antibiotics C. albicans can proliferate and invade tissues, leading to antibiotic‐associated candidal diarrhoea and inflammation of the mucosa (Gupta and Ehrinpreis, 1990; Danna et al ., 1991; Sanderson and Bukhari, 1991; Ponnuvel et al ., 1996; Hogenauer et al ., 1998; Krause et al ., 2001). The effects that bacteria of the host microflora have on C. albicans virulence are probably multifactorial, and may include elements such as competition for nutrients and host attachment sites, alteration of the local host environment, and the production of anti‐fungal compounds or chemicals that influence the morphological state of the fungus (Hoberg et al ., 1983). An understanding of the effects of bacteria on C. albicans growth and morphology will provide important insights into the physiology of the fungus within the host.…”

Candida Survival Strategies

“…In turn, bacteria have been shown to inhibit C. albicans filamentation by producing small signaling molecules, e.g., dodecanol and 3-oxo-C12-HSL from Pseudomonas aeruginosa, butyric acid from Lactobacillus rhamnosus, capric acid from Saccharomyces boulardii, cis-2-dodecenoic acid from Burkholderia cenocepacia, diffusible signal factor (DSF) from Xanthomonas campestris, and QSMs from Acinetobacter baumannii, Salmonella enterica Serovar Typhimurium, and Streptococcus mutans (Boon et al, 2008;Krasowska, Murzyn, Dyjankiewicz, Lukaszewicz, & Dziadkowiec, 2009;Murzyn, Krasowska, Stefanowicz, Dziadkowiec, & Lukaszewicz, 2010;Noverr & Huffnagle, 2004;Peleg et al, 2008;Tampakakis, Peleg, & Mylonakis, 2009;Wang et al, 2004). Lactobacillus spp., the most prevalent bacterial group in the female reproductive tract, as well as Enterococcus faecalis, a member of the GI-tract microbiota and an opportunistic pathogen, produce signaling molecules as metabolic byproducts (e.g., lactic acid, butyric acid), H 2 O 2 or organic acids that interfere with fungal adhesion, growth, adaptation or might influence the host immune response in an unfavorable way for C. albicans (Boris & Barbes, 2000;Braun, Hector, Kamark, Hart, & Cihlar, 1987;Cruz, Graham, Gagliano, Lorenz, & Garsin, 2013;Harriott & Noverr, 2011;Hoberg, Cihlar, & Calderone, 1983;Morales & Hogan, 2010;Noverr & Huffnagle, 2004;Strus et al, 2005;Wargo & Hogan, 2006). The necessary adaptations of C. albicans to these conditions are reflected in substantial changes in gene expression profiles when C. albicans is co-cultured with certain bacteria.…”