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Aucklandia lappa Causes Membrane Permeation of Candida albicans

Authors
Lee, Heung-ShickKim, Younhee
Issue Date
12월-2020
Publisher
KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
Keywords
Aucklandia lappa; Candida albicans; cell membrane; DPH; permeability
Citation
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY, v.30, no.12, pp.1827 - 1834
Indexed
SCIE
SCOPUS
KCI
Journal Title
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
Volume
30
Number
12
Start Page
1827
End Page
1834
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/51266
DOI
10.4014/jmb.2009.09044
ISSN
1017-7825
Abstract
Candida albicans is a major fungal pathogen in humans. In our previous study, we reported that an ethanol extract from Aucklandia lappa weakens C. albicans cell wall by inhibiting synthesis or assembly of both (1,3)-beta-D-glucan polymers and chitin. In the current study, we found that the extract is involved in permeabilization of C. albicans cell membranes. While uptake of ethidium bromide (EtBr) was 3.0% in control cells, it increased to 7.4% for 30 min in the presence of the A. lappa ethanol extract at its minimal inhibitory concentration (MIC), 0.78 mg/ml, compared to uptake by heat-killed cells. Besides, leakage of DNA and proteins was observed in A. lappa-treated C. albicans cells. The increased uptake of EtBr and leakage of cellular materials suggest that A. lappa ethanol extract induced functional changes in C. albicans cell membranes. Incorporation of diphenylhexatriene (DPH) into membranes in the A. lappa-treated C. albicans cells at its MIC decreased to 84.8%, after 60 min of incubation, compared with that of the controls, indicate that there was a change in membrane dynamics. Moreover, the anticandidal effect of theA. lappa ethanol extract was enhanced at a growth temperature of 40 degrees C compared to that at 35 degrees C. The above data suggest that the antifungal activity of the A. lappa ethanol extract against C. albicans is associated with synergistic action of membrane permeabilization due to changes in membrane dynamics and cell wall damage caused by reduced formation of (1,3)-beta-D-glucan and chitin.
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