Abstract

Monolaurin (also known as glycerol monolaurate) is a natural compound found in coconut oil and is known for its protective biological activities as an antimicrobial agent. The nature of oral candidiasis and the increased antifungal resistance demand the search for novel antifungal therapeutic agents. In this study, we examine the antifungal activity of monolaurin against Candida albicans biofilms (strain ATCC:SC5314/MYA2876) in vitro and investigate whether monolaurin can alter gene expression of host inflammatory cytokines, IL-1α and IL-1β. In a co-culture model, oral fibroblast cells were cultured simultaneously with C. albicans for 24 hrs followed by the exposure to treatments of monolaurin (3.9–2,500 µM), positive control fluconazole (32.2 µM), and vehicle control group (1% ethanol), which was a model used to evaluate the cytotoxicity of monolaurin on fibroblasts as well as to analyze morphological characteristics of biofilms through fluorescence microscopy. In addition, the co-culture model was used for RNA extraction of oral fibroblasts to assess gene expression of host inflammatory cytokines, using quantitative real-time PCR. Our results showed the MIC and MFC of monolaurin were in the range 62.5–125 µM and 125–250 µM, respectively. Biofilm antifungal assay showed significant reduction in Log (CFU/ml) of biofilms treated with 1,250 and 2,500 µM of 1-monolaurin when compared to the control groups . There was also a significant down-regulation of IL-1α and IL-1β in the co-culture treated with monolaurin. It can be concluded that monolaurin has a potential antifungal activity against C. albicans and can modulate the pro-inflammatory response of the host.

Highlights

  • Candida albicans is a prevalent opportunistic human fungal pathogen that lives commensally in the gut, oral pharyngeal, genito-urinary tract and skin

  • Susceptibility assay of 1-monolaurin showed antifungal activity against several strains of C. albicans in planktonic form, including a fluconazole-resistant strain 96901 in comparison to a standard antifungal agent, fluconazole (Table 1)

  • The minimum inhibitory concentration (MIC) and Minimum fungicidal concentration (MFC) were established to identify the concentrations needed to be applied to biofilms, which were in the range of ten times the MIC

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Summary

Introduction

Candida albicans is a prevalent opportunistic human fungal pathogen that lives commensally in the gut, oral pharyngeal, genito-urinary tract and skin. It may become pathogenic in immunocompromised patients or in individuals with an imbalance of competing bacterial microflora (Berman, 2012; Dovigo et al, 2011b; Neppelenbroek et al, 2006). The pathogenicity of the Candida species is attributed to critical virulence factors, such as adherence to surfaces (on both tissues and medical devices), biofilm formation, evasion of host immune defense mechanisms, and secretion of proteolytic enzymes, such as secreted aspartyl proteases (SAP) and phospholipases (Correia et al, 2010). Hyphal formation is considered the most critical factor involved in epithelial invasion and the degradation of epithelial cell junction proteins (Naglik et al, 2008; Villar et al, 2007)

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