Division of Gastroenterology and Hepatology, Department of Medicine, and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Gut Microbes. 2024 Jan-Dec;16(1):2421623. doi: 10.1080/19490976.2024.2421623. Epub 2024 Nov 5.
Undernutrition in children commonly disrupts the structure and function of the small intestinal microbial community, leading to enteropathies, compromised metabolic health, and impaired growth and development. The mechanisms by which diet and microbes mediate the balance between commensal and pathogenic intestinal flora remain elusive. In a murine model of undernutrition, we investigated the direct interactions , a prevalent small intestinal pathogen, on indigenous microbiota and specifically on Lactobacillus strains known for their mucosal and growth homeostatic properties. Our research reveals that colonization shifts the balance of lactic acid bacteria, causing a relative decrease in . and an increase in . This alteration corresponds with a decrease in multiple indicators of mucosal and nutritional homeostasis. Additionally, protein-deficient conditions coupled with infection exacerbate the rise of primary bile acids and susceptibility to bile acid-induced intestinal barrier damage. In epithelial cell monolayers, . mitigated bile acid-induced permeability, showing strain-dependent protective effects. , either alone or within a spp consortium, facilitated growth in protein-deficient mice, an effect attenuated by , despite not inhibiting Lactobacillus colonization. These results highlight Giardia's potential role as a disruptor of probiotic functional activity, underscoring the imperative for further research into the complex interactions between parasites and bacteria under conditions of nutritional deficiency.
儿童营养不良通常会破坏小肠微生物群落的结构和功能,导致肠病、代谢健康受损以及生长和发育受损。饮食和微生物如何调节共生和致病肠道菌群之间的平衡的机制仍不清楚。在营养不良的小鼠模型中,我们研究了普遍存在的小肠病原体 与土著微生物群,特别是与已知具有黏膜和生长稳态特性的乳杆菌菌株的直接相互作用。我们的研究表明, 定植会改变乳酸菌的平衡,导致相对减少 和增加 。这种变化与黏膜和营养稳态的多个指标的下降相对应。此外,蛋白质缺乏的条件加上 感染会加剧初级胆汁酸的增加和对胆汁酸诱导的肠道屏障损伤的易感性。在肠上皮细胞单层中, 减轻了胆汁酸诱导的通透性,显示出菌株依赖性的保护作用。 无论是单独存在还是在 spp 共生体中,都能促进蛋白质缺乏小鼠的生长,尽管 没有抑制乳杆菌定植,但这种作用会减弱。这些结果强调了 在营养缺乏条件下,作为益生菌功能活性破坏者的潜在作用,突显了进一步研究寄生虫和细菌之间复杂相互作用的必要性。