Boesenbergia rotunda extract decreases biofilm formation and host-pathogen interaction of bloodstream-isolated Candida albicans by interfering with biomolecule composition and metabolomics adaptation

Abstract

Boesenbergia rotunda (L.) Mansf. rhizome has been traditionally used to treat abscesses, leukoplakia, and leukorrhea. Candida albicans is a major cause of these incidences and can lead to bloodstream infection. This study aimed to evaluate the effectiveness and mechanisms of B. rotunda extract on susceptibility, biofilm formation, and invasion into human endothelial EA.hy926 cells of bloodstream-isolated C. albicans. Their virulence were determined by microdilution, metabolic activity, lactate dehydrogenase release, and internalization assays. Alterations in biomolecule composition were determined by Fourier-transform infrared microspectroscopy. The metabolomic profiles during host-pathogen interactions were assessed with high-resolution accurate-mass spectrometry. The B. rotunda extract consisted of 15.60% (w/w) pinostrobin and 6.02% (w/w) pinocembrin. All strains of C. albicans were not susceptible to the extract at a concentration of 100 μg/mL. The biofilm formation was inhibited only in C. albicans Isolate03 by the B. rotunda extract with IC50 value of 46.03 μg/mL. However, the ability of Isolate03 and Isolate04, invasive phenotypes, to damage the endothelial EA.hy926 cells was significantly inhibited with IC50 values of 27.39 and 30.81 μg/mL, respectively. The extract markedly altered the invasive phenotype's biomolecule composition and metabolomic profiles. The glycogen and carbohydrate compositions were decreased, whereas protein was increased. Moreover, propanoate and glycerolipid metabolism were dramatically regulated. These results suggest that alterations of biomolecule and metabolism could decrease their virulences because metabolic adaptation involved in pathogenic traits of C. albicans. Therefore, the B. rotunda extract might disrupt biomolecule compositions and metabolic pathways of the isolated C. albicans, thereby reducing biofilm formation and tissue invasion.