## 1 Introduction  
Vulvovaginal candidiasis (VVC) is a common fungal infection affecting the vulva and vagina, primarily caused by _Candida_ species [1]. It affects a significant proportion of women during their lifetime, with an estimated 75% of women experiencing at least one episode of VVC [2]. _C. albicans_, a yeast that is part of the normal vaginal microbiota, can overgrow and cause infection when the vaginal environment is disrupted, leading to an imbalance in microbial populations [3]. VVC interferes with a woman's daily life by causing severe itching, burning, pain during urination, and dyspareunia, which can decrease productivity and lead to psychological distress, frustration, and depression [4]. During pregnancy, it increases the risk of preterm birth and low birth weight, while in immunocompromised women, it can raise the risk of systemic infections [5]. _C. albicans_ adheres to vaginal epithelial cells using adhesion proteins and transitions from a yeast to a hyphal form, enhancing its tissue penetration ability [6]. It secretes hydrolytic enzymes such as aspartyl proteases (SAPs) and phospholipates that break down the epithelial barrier, inhibit complement activation, and impair macrophage and neutrophil activity, facilitating immune evasion [7]. Moreover, _Candida_ forms biofilms to escape antifungal treatment and immune defenses, and hyphal invasion activates inflammosomes, leading to the excessive release of pro-inflammatory cytokines such as IL-18, thereby exacerbating inflammation and tissue damage [8]. Elevated estrogen levels promote _Candida_ adhesion and hyphal growth, while the reduction in lactobacilli due to antibiotic use and immune suppression further facilitates infection [9]. To treat _C. albicans_ infections, antifungal agents are commonly employed, each with distinct mechanisms: azoles inhibit ergosterol production, a crucial component of the fungal cell membrane [10]; polyenes bind to ergosterol, forming pores in the membrane [11]; echinocandins prevent the synthesis of essential cell wall components [12]; and flucytosine disrupts DNA and RNA synthesis [13]. Although these treatments typically take several days to weeks to show effectiveness, they can cause side effects such as kidney or liver damage, and prolonged or excessive use may contribute to the development of resistance [14]. In response to these concerns, there is growing interest in exploring alternatives with fewer side effects and enhanced safety profiles [15]. In recent years, there has been growing interest in using probiotics as a complementary or alternative approach for treating or preventing VVC, with a focus on LAB due to their potential to restore the natural vaginal microbiota and inhibit _Candida_ overgrowth [16]. For instance, a study by [PERSON] et al. demonstrated that the administration of the _Lactobacillus rhuntosus_ GR1 and _Lactobacillus reuteri_ RC-14 strains significantly reduced the colonization of _C. albicans_ in the vaginal tract of women with recurrent VVC [17]. The authors showed that these probiotics produced lactic acid and hydrogen peroxide, which created an acidic environment hostile to _Candida_ growth. Moreover, Lactobacillus strains were observed to adhere to vaginal epithelial cells, forming a protective biofilm that limited _Candida_'s ability to colonize and infect the vaginal mucosa [18]. These findings underscore the role of probiotics in preventing VVC recurrence by balancing the vaginal microbiota and competing with _Candida_ for essential nutrients and binding sites [19]. Additionally, a study by [PERSON] et al. also confirmed that _Lactobacillus_ supplementation led to a significant reduction in the recurrence of VVC by restoring the vaginal microbiome and limiting _Candida_ overgrowth, further supporting the potential of probiotics as a therapeutic strategy for VVC [20].