作者列表：Yibing Lan, Cheng Wu, Peng Du, Jie Jiao, Chunming Li, Ketan Chu, Tao Zhang, Peiqiong Chen, An Li, Wenxian Xu, Xinyi Ying, Jianhong Zhou, Wenlong Lin, Linjuan Ma, Yizhou Huang

影响因子：3.8

期刊：Microbiology Spectrum

发表时间：2026-3-16

DOI:10.1128/spectrum.01669-25

文献主题：ABSTRACT

Our recent study showed that lat1, which encodes L-type amino acid transporter 1 (Lat1) was centrally positioned in the gene co-expression network of a Candida albicans (C. albicans) infection model of cell culture and suggested that this gene might play a critical role in the pathogenesis of C. albicans infections. In the current work, we used CRISPR-Cas9 to generate a C. albicans lat1 mutant strain (lat1Δ/Δ), using C. albicans SC5314 as the wild-type (WT) strain. An in vitro Candida infection model using vaginal epithelial cells and a murine model of vulvovaginal candidiasis was used to investigate the role of lat1 in the pathogenicity of C. albicans. It was found that lat1 played important roles in cell proliferation, morphogenesis, early adherence, and biofilm formation of C. albicans. VK2-E6E7 human vaginal epithelial cells infected with the lat1Δ/Δ mutant strain also showed significantly lower activation of Toll-like receptor 2/4 (TLR2/4) and the downstream MyD88/NF-κB signaling pathway, accompanied by an attenuated secretion of inflammatory cytokines. In the murine model of vulvovaginal candidiasis, infection caused by lat1Δ/Δ showed a lower fungal burden in the vaginal lavage fluid, reduced production of inflammatory cytokines, and diminished recruitment of neutrophils to the vaginal epithelium, relative to that caused by the WT strain. Based on these findings, we conclude that lat1 plays an important role in the host-pathogen interactions in C. albicans infections by impacting the virulence of C. albicans and host inflammatory responses; the latter was possibly via the TLR2/4-MyD88-NF-κB pathway.