title: Arachidonic acid affects biofilm formation and PGE2 level in Candida albicans and non-albicans species in presence of subinhibitory concentration of fluconazole and terbinafine.
abstract: Candida albicans utilizes arachidonic acid (AA) released during the course of infection (Candidiasis) from phospholipids of infected host cell membranes and synthesizes extracellular prostaglandin(s) which play an important role in hyphae formation and host cell damage. C. albicans biofilms secrete significantly more prostaglandin(s) and evidence suggests that Candida biofilms have dramatically reduced susceptibility to majority of antifungal drugs. AA influences the saturation level of lipids and fluidity of yeast cell membranes. Therefore the aim of this study was to evaluate the effect of AA alone or in combination with antifungal agents on biofilm formation and production of prostaglandin (PGE2) in C. albicans, C. parapsilosis, C. glabrata, C. tropicalis, and C. albicans amphotericin B resistant strain (AmBR). Maximum biofilm formation was found to be in the case of C. albicans compared to C. non-albicans species. However, among the non-albicans species C. tropicalis exhibited highest biofilm formation. Treatment with AA in combination with subinhibitory concentrations of fluconazole and terbinafine separately exhibited significant (p<0.05) reduction in biofilm formation against C. glabrata, C. parapsilosis, C. tropicalis and AmBR as compared to their individual effect. Further, these two antifungal agents in combination with AA caused an increase in production of prostaglandin from fungal cell itself which was significant (p<0.05) in case of all the strains tested.
authors.affiliation: Medical Mycology Lab, Division of Fermentation Technology, CSIR-Central Drug Research Institute, B.S. 10/1, Sector 10, Jankipuram Extension, Sitapur Road, Lucknow 226021, India; Department of Biochemistry, Jamia Hamdard, New Delhi, India.
authors.forename: Nripendra Nath
authors.initials: NN
authors.lastname: Mishra
authors.affiliation: Department of Biochemistry, Jamia Hamdard, New Delhi, India.
authors.forename: Shakir
authors.initials: S
authors.lastname: Ali
authors.affiliation: Medical Mycology Lab, Division of Fermentation Technology, CSIR-Central Drug Research Institute, B.S. 10/1, Sector 10, Jankipuram Extension, Sitapur Road, Lucknow 226021, India. Electronic address: pk_shukla@cdri.res.in.
authors.forename: Praveen K
authors.initials: PK
authors.lastname: Shukla
mesh_terms: D000935:Antifungal Agents / Q000494:pharmacology*; D016718:Arachidonic Acid / Q000494:pharmacology*; D018441:Biofilms / Q000187:drug effects* / Q000254:growth & development; D002175:Candida / Q000737:chemistry / Q000145:classification / Q000187:drug effects*; D002176:Candida albicans / Q000187:drug effects; D015232:Dinoprostone / Q000032:analysis*; D015725:Fluconazole / Q000494:pharmacology*; D008826:Microbial Sensitivity Tests; D008856:Microscopy, Fluorescence; D009281:Naphthalenes / Q000494:pharmacology*; D000077291:Terbinafine
chemical_list: D000935:Antifungal Agents; D009281:Naphthalenes; D016718:Arachidonic Acid; D015725:Fluconazole; D000077291:Terbinafine; D015232:Dinoprostone
keywords: AmBR; Arachidonic acid; Candida albicans; Candida tropicalis; FDA; Prostaglandin E2