Candida auris has emerged as a medically important pathogen with considerable resistance to antifungal agents. The ability to produce biofilms is an important pathogenicity feature of this species that aids escape of host immune responses and antimicrobial agents. The objective of this study was to verify antifungal action using in vitro and in vivo models of the Lactobacillus paracasei 28.4 probiotic cells and postbiotic activity of crude extract (LPCE) and fraction 1 (LPF1), derived from L. paracasei 28.4 supernatant. Both live cells and cells free supernatant of L. paracasei 28.4 inhibited C. auris suggesting probiotic and postbiotic effects. The minimum inhibitory concentration (MIC) for LPCE was 15 mg/mL and ranges from 3.75 to 7.5 mg/mL for LPF1. Killing kinetics determined that after 24 h treatment with LPCE or LPF1 there was a complete reduction of viable C. auris cells compared to fluconazole, which decreased the initial inoculum by 1-logCFU during the same time period. LPCE and LPF1 significantly reduced the biomass (p = 0.0001) and the metabolic activity (p = 0.0001) of C. auris biofilm. There was also a total reduction (~10⁸ CFU/mL) in viability of persister C. auris cells after treatment with postbiotic elements (p < 0.0001). In an in vivo study, injection of LPCE and LPF1 into G. mellonella larvae infected with C. auris prolonged survival of these insects compared to a control group (p < 0.05) and elicited immune responses by increasing the number of circulating hemocytes and gene expression of antimicrobial peptide galiomicin. We concluded that the L. paracasei 28.4 cells and postbiotic elements (LPCE and LPF1) have antifungal activity against planktonic cells, biofilms, and persister cells of C. auris. Postbiotic supplementation derived from L. paracasei 28.4 protected G. mellonella infected with C. auris and enhanced its immune status indicating a dual function in modulating a host immune response.

念珠菌已成为医学上重要的病原体，对抗真菌剂具有相当大的抵抗力。产生生物膜的能力是该物种的一个重要致病性特征，有助于逃避宿主免疫反应和抗菌剂。本研究的目的是验证使用的抗真菌作用体外和体内的模型副干酪乳杆菌28.4 粗提物 (LPCE) 和部分 1 (LPF1) 的益生菌细胞和后生元活性，来源于副干酪乳杆菌28.4 上清液。活细胞和细胞游离上清液副干酪乳杆菌28.4 抑制耳念珠菌提示益生菌和后生元效应。LPCE 的最小抑制浓度 (MIC) 为 15 mg/mL，LPF1 的范围为 3.75 至 7.5 mg/mL。杀伤动力学确定，在用 LPCE 或 LPF1 处理 24 小时后，活细胞完全减少耳念珠菌细胞与氟康唑相比，氟康唑在同一时间段内将初始接种量减少了 1-logCFU。LPCE 和 LPF1 显着降低了生物量（p= 0.0001) 和代谢活动 (p= 0.0001) 的耳念珠菌生物膜。持久性细胞的生存能力也完全降低 (~10 ^{8 CFU/mL)}耳念珠菌后生元处理后的细胞（p< 0.0001）。在一个体内研究，将 LPCE 和 LPF1 注入大蜡螟感染的幼虫耳念珠菌与对照组相比，这些昆虫的存活时间更长（p< 0.05) 并通过增加循环血细胞的数量和抗菌肽 galiomicin 的基因表达来引发免疫反应。我们的结论是副干酪乳杆菌28.4 细胞和后生元元素（LPCE 和 LPF1）对浮游细胞、生物膜和持久细胞具有抗真菌活性耳念珠菌. 后生元补充剂源自副干酪乳杆菌28.4 受保护大蜡螟感染耳念珠菌并增强其免疫状态，表明在调节宿主免疫反应方面具有双重功能。