空肠弯曲杆菌(C.jejuni)是全球食源性感染的最常见原因之一,也是腹泻疾病的主要原因。本研究旨在探讨肠道共生菌控制空肠弯曲菌感染的能力。体外筛选了来自肉鸡肠粘膜的细菌菌株。空肠弯曲杆菌ATCCBAA1153。唾液杆菌UO的无细胞上清液(CFS)。C249对病原体显示出有效的剂量依赖性抗菌活性,可能是由于细菌素样部分的存在,通过蛋白酶处理证实。基因组和外蛋白质组分析揭示了已知细菌素的存在,包括Abp118.Lg的基因组。唾液UO。C249具有1.8Mb染色体和203kb大质粒。该菌株对几种抗生素敏感,在模拟鸡胃肠道(GIT)中具有较高的存活率。蛋白酶后处理显示出残留的抑制活性,建议替代抗菌机制。短链脂肪酸(SCFA)定量证实乙酸的非抑制性水平(24.4±1.2mM),异戊酸(34±1.0µM),和丁酸(32±2.5µM)。有趣的是,从Lg的CFS分离的细胞外囊泡(EV)。唾液UO。发现C249抑制空肠弯曲杆菌ATCCBAA-1153。这些EV的蛋白质组分析揭示了与CFS中鉴定的细菌素不同的独特蛋白质的存在。在电动汽车中鉴定的大多数蛋白质位于膜中,并在跨膜运输和肽聚糖降解中发挥作用,肽酶,蛋白水解,和水解。这些发现表明,尽管细菌素是一种主要的抗菌机制,EV的产生也有助于Lg的抑制活性。唾液UO。C249对抗空肠杆菌。
目标:空肠弯曲杆菌(C.jejuni)是胃肠炎的主要原因,也是全球公共卫生问题。家畜生产中抗生素耐药性的增加和有效替代品的缺乏对控制空肠弯曲杆菌感染提出了严峻的挑战。因此,需要替代策略来控制这种病原体,特别是在家禽业中,它很普遍,可以通过受污染的食品传播给人类。在这项研究中,唾液小杆菌UO。从肉鸡肠粘膜分离的C249抑制空肠弯曲杆菌并表现出重要的益生菌特征。除了细菌素,Lg.唾液UO。C249分泌具有不同于细菌素的独特蛋白质组的抗微生物细胞外囊泡(EV),其参与跨膜转运和肽聚糖降解。我们的发现表明,除了细菌素,EV产生也是Lg使用的独特的抑制性信号传导机制。唾液UO。C249控制空肠杆菌。这些发现为益生菌电动汽车在病原体控制中的应用提供了希望。
Campylobacter jejuni (C. jejuni) is one of the most common causes of foodborne infections worldwide and a major contributor to diarrheal diseases. This study aimed to explore the ability of commensal gut bacteria to control C. jejuni infection. Bacterial strains from the intestinal mucosa of broilers were screened in vitro against C. jejuni ATCC BAA1153. The cell-free supernatant (CFS) of Ligilactobacillus salivarius UO.C249 showed potent dose-dependent antimicrobial activity against the pathogen, likely due to the presence of bacteriocin-like moieties, as confirmed by protease treatment. Genome and exoproteome analyses revealed the presence of known
bacteriocins, including Abp118. The genome of Lg. salivarius UO.C249 harbors a 1.8-Mb chromosome and a 203-kb megaplasmid. The strain was susceptible to several antibiotics and had a high survival rate in the simulated chicken gastrointestinal tract (GIT). Post-protease treatment revealed residual inhibitory activity, suggesting alternative antimicrobial mechanisms. Short-chain fatty acid (SCFA) quantification confirmed non-inhibitory levels of acetic (24.4 ± 1.2 mM), isovaleric (34 ± 1.0 µM), and butyric (32 ± 2.5 µM) acids. Interestingly, extracellular vesicles (EVs) isolated from the CFS of Lg. salivarius UO.C249 were found to inhibit C. jejuni ATCC BAA-1153. Proteome profiling of these EVs revealed the presence of unique proteins distinct from
bacteriocins identified in CFS. The majority of the identified proteins in EVs are located in the membrane and play roles in transmembrane transport and peptidoglycan degradation, peptidase, proteolysis, and hydrolysis. These findings suggest that although
bacteriocins are a primary antimicrobial mechanism, EV production also contributes to the inhibitory activity of Lg. salivarius UO.C249 against C. jejuni.
OBJECTIVE: Campylobacter jejuni (C. jejuni) is a major cause of gastroenteritis and a global public health concern. The increasing antibiotic resistance and lack of effective alternatives in livestock production pose serious challenges for controlling C. jejuni infections. Therefore, alternative strategies are needed to control this pathogen, especially in the poultry industry where it is prevalent and can be transmitted to humans through contaminated food products. In this study, Ligilactobacillus salivarius UO.C249 isolated from broiler intestinal mucosa inhibited C. jejuni and exhibited important probiotic features. Beyond
bacteriocins, Lg. salivarius UO.C249 secretes antimicrobial extracellular vesicles (EVs) with a unique protein set distinct from bacteriocins that are involved in transmembrane transport and peptidoglycan degradation. Our findings suggest that beyond
bacteriocins, EV production is also a distinct inhibitory signaling mechanism used by Lg. salivarius UO.C249 to control C. jejuni. These findings hold promise for the application of probiotic EVs for pathogen control.