AI Article Synopsis
- Candida albicans is a serious pathogen causing numerous infections, with its virulence largely linked to the peptide candidalysin (CL), which damages epithelial cells.
- CL triggers a response by forming pores in cell membranes, activating cell signaling pathways via the epidermal growth factor receptor, but previous reviews haven't fully explored how CL inflicts membrane damage.
- Recent research revealed that CL undergoes a unique self-assembly process before membrane infiltration, and the discovery of CL variants in other Candida species may lead to better therapeutic strategies against infections.
Article Abstract
Candida albicans is a deadly pathogen responsible for millions of mucosal and systemic infections per year. The pathobiology of C. albicans is largely dependent on the damaging and immunostimulatory properties of the peptide candidalysin (CL), a key virulence factor. When CL forms pores in the plasma membrane of epithelial cells, it activates a response network grounded in activation of the epidermal growth factor receptor. Prior reviews have characterized the resulting CL immune activation schemas but lacked insights into the molecular mechanism of CL membrane damage. We recently demonstrated that CL functions by undergoing a unique self-assembly process; CL forms polymers and loops in aqueous solution prior to inserting and forming pores in cell membranes. This mechanism, the first of its kind to be observed, informs new therapeutic avenues to treat Candida infections. Recently, variants of CL were identified in other Candida species, providing an opportunity to identify the residues that are key for CL to function. In this review, we connect the ability of CL to damage cell membranes to its immunostimulatory properties.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9852700 | PMC |
| http://dx.doi.org/10.1016/j.jbc.2022.102829 | DOI Listing |
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