Experimental Biofilm-Related
            <i>Candida</i>
            Infections

Cirasola, Daniela; Sciota, Rita; Vizzini, Loredana; Ricucci, Valentina; Morace, Giulia; Borghi, Elisa

doi:10.2217/fmb.13.36

Cited by 27 publications

(32 citation statements)

References 30 publications

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“…The pathogenicity of C. albicans, in the presence and absence of ACh, was assessed using the G. mellonella killing assay (20,21). Sixth-instar G. mellonella larvae (Livefoods Direct, Ltd., United Kingdom) with a body weight of between 200 to 300 mg were used in the study.…”

Section: Methodsmentioning

confidence: 99%

Acetylcholine Protects against Candida albicans Infection by Inhibiting Biofilm Formation and Promoting Hemocyte Function in a Galleria mellonella Infection Model

et al. 2015

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dBoth neuronal acetylcholine and nonneuronal acetylcholine have been demonstrated to modulate inflammatory responses. Studies investigating the role of acetylcholine in the pathogenesis of bacterial infections have revealed contradictory findings with regard to disease outcome. At present, the role of acetylcholine in the pathogenesis of fungal infections is unknown. Therefore, the aim of this study was to determine whether acetylcholine plays a role in fungal biofilm formation and the pathogenesis of Candida albicans infection. The effect of acetylcholine on C. albicans biofilm formation and metabolism in vitro was assessed using a crystal violet assay and phenotypic microarray analysis. Its effect on the outcome of a C. albicans infection, fungal burden, and biofilm formation were investigated in vivo using a Galleria mellonella infection model. In addition, its effect on modulation of host immunity to C. albicans infection was also determined in vivo using hemocyte counts, cytospin analysis, larval histology, lysozyme assays, hemolytic assays, and real-time PCR. Acetylcholine was shown to have the ability to inhibit C. albicans biofilm formation in vitro and in vivo. In addition, acetylcholine protected G. mellonella larvae from C. albicans infection mortality. The in vivo protection occurred through acetylcholine enhancing the function of hemocytes while at the same time inhibiting C. albicans biofilm formation. Furthermore, acetylcholine also inhibited inflammation-induced damage to internal organs. This is the first demonstration of a role for acetylcholine in protection against fungal infections, in addition to being the first report that this molecule can inhibit C. albicans biofilm formation. Therefore, acetylcholine has the capacity to modulate complex host-fungal interactions and plays a role in dictating the pathogenesis of fungal infections.

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Section: Methodsmentioning

confidence: 99%

Acetylcholine Protects against Candida albicans Infection by Inhibiting Biofilm Formation and Promoting Hemocyte Function in a Galleria mellonella Infection Model

et al. 2015

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“…For further experiments, we used the inoculum of 10 5 CFU/larva. isolates used in a previous work [18]. *p < 0.05; **p < 0.01; ***p < 0.001.…”

Section: • • In Vitro Biofilm Modelmentioning

confidence: 95%

“…All fungal strains were stored at -80°C until use and grown overnight in yeast extract, peptone, dextrose (1% w/v yeast extract, 2% w/v peptone, 2% w/v dextrose) liquid medium (YPD) at 30°C with agitation before experiments. Protocols for inoculum preparation and biofilm growth followed those described previously [17,18] using 96-well polystyrene plates. Briefly, strains were grown overnight in YPD broth at 30°C in an orbital shaker at 150 rpm.…”

Section: • • C Albicans Isolatesmentioning

confidence: 99%

Correlation Between Candida Albicans Biofilm Formation and Invasion of the Invertebrate Host Galleria Mellonella

et al. 2014

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“…In the Galleria mellonella (wax moth) larvae model, which has a similar immune response to mammals, fi ve biofi lm-producing and four non-biofi lm forming invasive human clinical isolates of C. albicans were used to assess virulence. Biofi lm formation signifi cantly decreased survival time of the infected larvae, with 80 % of larvae infected by biofi lm-forming C. albicans dying by 72 h (Cirasola et al 2013 ). An additional study utilized the Galleria mellonella model to examine the role of biofi lm formation in virulence among 20 human clinical isolates 15 bloodstream and 5 catheter-related, 9 biofi lm-forming) of C. albicans (Borghi et al 2014 ).…”

Section: Biofi Lms In Clinical Isolates Of Candida Sppmentioning

confidence: 99%

Biofilm Formation by Clinical Isolates and Its Relevance to Clinical Infections

Akers

Cardile

Wenke

et al. 2014

Advances in Experimental Medicine and Biology

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Reports of biofilms have increased exponentially in the scientific literature over the past two decades, yet the vast majority of these are basic science investigations with limited clinical relevance. Biofilm studies involving clinical isolates are most often surveys of isolate collections, but suffer from lack of standardization in methodologies for producing and assessing biofilms. In contrast, more informative clinical studies correlating biofilm formation to patient data have infrequently been reported. In this chapter, biofilm surveys of clinical isolates of aerobic and anaerobic bacteria, mycobacteria, and Candida are reviewed, as well as those pertaining to the unique situation of cystic fibrosis. In addition, the influence of host components on in vitro biofilm formation, as well as published studies documenting the clinical impact of biofilms in human infections, are presented.

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Experimental Biofilm-Related Candida Infections

Cited by 27 publications

References 30 publications

Acetylcholine Protects against Candida albicans Infection by Inhibiting Biofilm Formation and Promoting Hemocyte Function in a Galleria mellonella Infection Model

Acetylcholine Protects against Candida albicans Infection by Inhibiting Biofilm Formation and Promoting Hemocyte Function in a Galleria mellonella Infection Model

Correlation Between Candida Albicans Biofilm Formation and Invasion of the Invertebrate Host Galleria Mellonella

Biofilm Formation by Clinical Isolates and Its Relevance to Clinical Infections

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