## 4 Discussion  
Our results indicate that _Weissella confusa_ WIKIM51 (Wilac D001) exhibits antifungal activity by inhibiting the formation of _C. albicans_ biofilm. Pro\(-\)inflammatory cytokines, including IL\(-\)6 and IL\(-\)8, were upregulated by _C. albicans_ infection in VECs; however, they were significantly downregulated by Wilac D001. The inhibitory effect of Wilac D001 against the growth of _C. albicans_ was similar to that of _L. reuteri_ and _L. rhamnus_. These results propose that the antifungal effects of Wilac D001 against _C. albicans_ are comparable to those of _L. reuteri_ and _L. rhamnus_. In particular, Wilac D001 exhibits a significantly higher efficiency in regulating pro\(-\)inflammatory cytokines than _L. reuteri_ and _L. rhamnus_. A vaginal environment dominated by _Lactobacillus_ spp. is crucial for protecting the genital tract from opportunistic infections [4]. _Lactobacillus_ produces lactic acid to maintain an acidic environment and inhibits the growth of other microorganisms as well as the influx of pathogens [4; 25]. A lack of lactobacilli in the vagina is associated with infections caused by _Candida_ spp., an opportunistic pathogen. Several gynecologic diseases, including pelvic inflammatory disease (PIV), sensitivity to human immunodeficiency virus (HIV), and even adverse pregnancy outcomes, such as the preterm premature rupture of membranes (PPROMs) and preterm birth (PTB), are associated with the proportion of lactobacilli in the vagina [30; 31; 32]. Here, we have investigated the antifungal effect of Wilac D001, which was isolated from dandelion kimchi, against _C. albicans_ on vascular endothelial cells for the first time. There is concern about the safety of the _Weissella_ genus due to potential pathogenicity [33]. Some studies report that certain strains of _W. confusa_ may cause infections, particularly in immunocompromised patients [34; 35]. However, other _W. confusa_ strains show promise in mitigating gut dysbiosis linked to inflammatory bowel disease and cancers, with demonstrated benefits in maintaining intestinal tight junctions and modulating intestinal cell responses [19; 35; 36]. Therefore, the precise taxonomic category is crucial for understanding its potential pathogenicity. The strain that we used in this experiment is Wilac D001, which is a non\(-\)spore\(-\)forming, Gram\(-\)positive coccobacillus that has obtained safety approval from the FDA. Wilac D001 has been annotated by the National Center for Biotechnology Information (NCBI, CP110106). The biofilm formation is the essential mechanism underlying _C. albicans_ infection; it enhances pathogenicity through increased colonization and microbial adherence [37]. Adhesion to the surface of the epithelial cell is pivotal to the constant colonization of _C. albicans_[26; 38]. Hyphae\(-\)morphological colonization was observed in vaginal epithelial cells infected with _C. albicans_. However, Wilac D001 protected VECs by blocking the congregation of _C. albicans_ on VECs. _Lactobacillus_ spp. also reduced the adhesion of _C. albicans_ to VECs surfaces by competing for adhesion sites, as reported [39]. The expression of pro\(-\)inflammatory cytokines, including IL\(-\)6 and IL\(-\)8, is upregulated in VECs, owing to _C. albicans_ infection [40]. Furthermore, a clinical study demonstrated that the concentration of IL\(-\)8 was higher in women infected with _Candida_ spp. [41]. Our data indicated that Wilac D001 significantly reduced the production of both IL\(-\)6 and IL\(-\)8 in VECs infected with _C. albicans_. A previous study reports that the response of inflammatory expressions to lipopolysaccharide stimulation can be reduced in a mild acidic environment (pH 5.5\(-\)6.0) [42]. However, we did not analyze culture media pH