Abstract
Candida sp. impelled opportunistic infection in immune-compromised patients ensuing from asymptomatic colonization to pathogenic forms. Moreover, slow spread of Candida species inducing refractory mucosal and invasive infections brings acute resistance to antifungal drugs. Hence, here we probed the effect of encapsulated preparation of cinnamaldehyde (CNMA) in multilamellar liposomes (ML) against Candida albicans. The efficacy of ML-CNMA against Candida biofilm was assessed by scanning electron microscopy, transmission electron microscopy, as well as light microscopy and its percent inhibition, was determined by XTT [2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] and crystal violet assay. ML-CNMA showed more fungicidal activity than free CNMA as well as multilamellar liposomal amphotericin B (ML-Amp B), which was further confirmed by spot test assay and Log-logistic dose–response analysis. Antifungal activity was driven by reactive oxygen species and cellular damage by sustained release of CNMA. Effect on hyphal formation during 48 h in presence/absence of ML-CNMA was observed under a microscope and further substantiated by RT-PCR by amplifying HWP1, the gene responsible for hyphal wall protein formation. Apoptotic programmed cell death was analyzed by FACS analysis which was further confirmed by cytochrome C release assay. This study elucidates the mechanistic insight of the enhanced antifungal activity of ML preparation of CNMA against Candida infections.
Highlights
The threat of developing HIV-related complications differs with the extent of immunosuppression in patients (Wadhwa et al, 2007)
For the quantification of entrapped drugs, liposomes were ruptured by treatment with 0.1% sodium deoxycholate and released drugs concentration were calculated by comparison with standard calibration graphs (for released amphotericin B (Amp B); calculations based on UV-Vis absorption vs. drug concentrations, see Supplementary Figure S1, and for released CNMA; calculations based on colony forming unit [CFU = log10 vs. CNMA concentrations], see Supplementary Figure S2)
The comprehensive susceptibilities/resistant of clinical isolates were enlisted in the tabular form (Figure 1D), where minimum inhibitory concentration (MIC) break point of Amp B taken according to CLSI 2008 guideline (Clinical and Laboratory Standards Institute, 2008) and CNMA break point was ≥550 mg·l−1 (MIC against C. albicans ATCC 24433)
Summary
The threat of developing HIV-related complications differs with the extent of immunosuppression in patients (Wadhwa et al, 2007). Candida albicans is a pathogen, causing a multitude of oral and vaginal infections to severe systemic disorders in immune compromised patients (Fidel, 2006; Perlroth et al, 2007). It forms biofilms, an organized and highly structured community of cells (Jin et al, 2005; Ramage et al, 2005), which lately enhanced resistance against antimicrobial agents as well as to host defenses, with profound clinical implications (Costerton et al, 1999; Donlan, 2001; Khan and Khan, 2016). Candida infections are getting resistant to fluconazole and amphotericin B (Amp B; Pfaller, 1996; Mah and O’Toole, 2001).
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