TY - JOUR
T1 - Regulation of DAF-16-mediated longevity and immune response to Candida albicans infection in Caenorhabditis elegans
AU - Kitisin, Thitinan
AU - Muangkaew, Watcharamat
AU - Sukphopetch, Passanesh
N1 - Publisher Copyright:
©2022 by EDIMES - Edizioni Internazionali Srl. All rights reserved.
PY - 2022/1
Y1 - 2022/1
N2 - 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.
AB - 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.
KW - Caenorhabditis elegans
KW - Candida albicans
KW - DAF-16
KW - immune response
KW - insulin/IGF-1-like signaling (IIS) pathway
KW - longevity
UR - http://www.scopus.com/inward/record.url?scp=85127898697&partnerID=8YFLogxK
M3 - Article
C2 - 35403847
AN - SCOPUS:85127898697
SN - 1121-7138
VL - 45
SP - 51
EP - 61
JO - New Microbiologica
JF - New Microbiologica
IS - 1
ER -