Anandamide prevents the adhesion of filamentous Candida albicans to cervical epithelial cells

Ronit Vogt Sionov*, Mark Feldman, Reem Smoum, Raphael Mechoulam, Doron Steinberg

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

Candidiasis is a fungal infection caused by Candida species that have formed a biofilm on epithelial linings of the body. The most frequently affected areas include the vagina, oral cavity and the intestine. In severe cases, the fungi penetrate the epithelium and cause systemic infections. One approach to combat candidiasis is to prevent the adhesion of the fungal hyphae to the epithelium. Here we demonstrate that the endocannabinoid anandamide (AEA) and the endocannabinoid-like N-arachidonoyl serine (AraS) strongly prevent the adherence of C. albicans hyphae to cervical epithelial cells, while the endocannabinoid 2-arachidonoylglycerol (2-AG) has only a minor inhibitory effect. In addition, we observed that both AEA and AraS prevent the yeast-hypha transition and perturb hyphal growth. Real-time PCR analysis showed that AEA represses the expression of the HWP1 and ALS3 adhesins involved in Candida adhesion to epithelial cells and the HGC1, RAS1, EFG1 and ZAP1 regulators of hyphal morphogenesis and cell adherence. On the other hand, AEA increased the expression of NRG1, a transcriptional repressor of filamentous growth. Altogether, our data show that AEA and AraS have potential anti-fungal activities by inhibiting hyphal growth and preventing hyphal adherence to epithelial cells.

Original languageAmerican English
Article number13728
JournalScientific Reports
Volume10
Issue number1
DOIs
StatePublished - 1 Dec 2020

Bibliographical note

Funding Information:
This study was partially supported by Agriculture Ministry of Israel. We are grateful to Dr. Yael Feinstein-Rotkopf for operating the Nikon spinning scan microscope at our Interdepartment Core Research Facility. We thank Muna Aqawi and Sarah Gingichashvili for their support.

Publisher Copyright:
© 2020, The Author(s).

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