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- REVIEW] Candida albicans, a Major Human Fungal Pathogen
- Joon Kim , Peter Sudbery
- J. Microbiol. 2011;49(2):171-177. Published online May 3, 2011
- DOI: https://doi.org/10.1007/s12275-011-1064-7
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- 373 Scopus
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Abstract
- Candida albicans is the most common human fungal pathogen (Beck-Sague and Jarvis, 1993). It is normally a harmless commensal organism. However, it is a opportunistic pathogen for some immunologically weak and immunocompromised people. It is responsible for painful mucosal infections such as the vaginitis in women and oral-pharangeal thrush in AIDS patients. In certain groups of vulnerable patients it causes severe, life-threatening bloodstream infections and it causes severe, life-threatening bloodstream infections and subsequent infections in the internal organs. There are various fascinating features of the C. albicans life cycle and biology that have made the pathogen the subject of extensive research, including its ability to grow in unicellular yeast, psudohyphal, and hyphal forms (Fig. 1A); its ability to switch between different but stable phenotypic states, and the way that it retains the ability to mate but apparently loses the ability to go through meiosis to complete the sexual cycle. This research has been greatly facilitated by the derivation of the complete C. albicans genome sequence (Braun et al., 2005), the development of a variety of molecular tools for gene manipulation, and a store of underpinning knowledge of cell biology borrowed from the distantly related model yeast Saccharomyces cerevisiae (Berman and Sudbery, 2002; Noble and Johnson, 2007). This review will provide a brief overview of the importance of C. albicans as a public health issue, the experimental tools developed to study its fascinating biology, and some examples of how these have been applied.
- Morphological changes of biomembranes by amphiphilic basic peptides mastoparan B and 4₃
- Park, Nam Gyu , Kim, Chan Hee , Chung, Joon Ki , Huh, Min Do , Park, Jang Su , Kang, Shin Won
- J. Microbiol. 1998;36(3):179-183.
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Abstract
- We investigated the modes interaction of mastoparan B, model peptide Ac-(Leu-Ala-Arg-Leu)_3-NHCH_3 (4_3) and gramicidin S, amphiphilic peptides with biomembranes. As a result, we observed morphological changes in erythrocytes and bacterial membranes. Mastoparan B caused a change in the shape of erythrocytes from normal discoid to a crenated form (named echinocytes). The major morphological changes of Staphylococcus aureus 209P induced by 4_3 and gramicidin S were the destruction of the cell wall and the accumulation of large enectron-opaque structures in the ccytoplasm. The damage was initiated by gap formation in the cell wall. In the freeze-fracture method, heavy damages occurred in the cell membrane. The cell wall became thin and finally ruptured. The protoplasts prepared from the 4_3-treated bacteria were unstable in an osmotically controlled vuffer and lysed within 2 hr, whereas those prepared from control cell and 4_3treated protoplasts were stable for more than 3 hr. These structural changes were not specific for 4_3 but were also found in gramicidin S-treated cells. Therefore, we expect that the bactericidal mechanism of 4_3, an amphiphilic linear peptide, and gramicidin S, an amphiphilic cyclic peptide, on Staphylococcus aureus 209P will by basically the same. In the case of erythrocytes, their transformation to echinocytes by mastoparan B should be similar to the way in which the transformation is caused by amphiphilic basic peptides such 4_3 and gramicidin S.
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