Regulation of DAF-16-mediated longevity and immune response to Candida albicans infection in Caenorhabditis elegans
6
Issued Date
2022-01-01
Resource Type
ISSN
11217138
Scopus ID
2-s2.0-85127898697
Pubmed ID
35403847
Journal Title
New Microbiologica
Volume
45
Issue
1
Start Page
51
End Page
61
Rights Holder(s)
SCOPUS
Bibliographic Citation
New Microbiologica Vol.45 No.1 (2022) , 51-61
Suggested Citation
Kitisin T. Regulation of DAF-16-mediated longevity and immune response to Candida albicans infection in Caenorhabditis elegans. New Microbiologica Vol.45 No.1 (2022) , 51-61. 61. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/86609
Title
Regulation of DAF-16-mediated longevity and immune response to Candida albicans infection in Caenorhabditis elegans
Author(s)
Author's Affiliation
Other Contributor(s)
Abstract
Candida albicans can cause infections ranging from superficial skin infections to life-threatening systemic infections in immunocompromised hosts. Although several C. albicans virulence factors are widely discussed in great detail, intrinsic host determinants that are critical for C. albicans pathogenesis remain less interested and poorly understood. In view of this, a model of Caenorhabditis elegans was used to study host longevity and immunity in response to C. albicans pathogenesis. The influence of C. albicans in pathological and survival aspects was evaluated using C. elegans. C. albicans hyphal formation in different C. elegans genetic backgrounds was evaluated. Moreover, several C. elegans fluorescent proteins as gene expression markers upon C. albicans infections were evaluated. C. albicans is pathogenic to C. elegans and reduces the lifespan of C. elegans in association with repression of the insulin/IGF-1-like signaling (IIS) pathway. Moreover, repression of DAF-16/forkhead transcription factor increases aggressiveness of C. albicans by enhancing hyphal formation. In addition, infection of C. albicans increases lipofuscin accumulation, promotes DAF-16 nuclear translocation, increases superoxide dismutase (SOD-3) expression, which coordinately links between aging and innate immunity. Thus, we demonstrate here the strategy to utilize C. elegans as a model host to elucidate host genetic determinants that provide insights into the pathogenesis of C. albicans infections.