Medical Proteomics Unit, Research Department, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand.
Department of Dermatology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand.
Microbiome. 2024 Sep 17;12(1):175. doi: 10.1186/s40168-024-01877-y.
Lactobacillus acidophilus is a commensal urinary bacterium found more abundantly in healthy individuals than in stone patients. Hence, it has been proposed to play an inhibitory role in kidney stone disease (KSD) but with unclear mechanisms. We therefore investigated the direct effects of L. acidophilus on calcium oxalate (CaOx) stone development compared with Escherichia coli, which is known to promote CaOx stone formation.
L. acidophilus at 1 × 10 CFU/ml significantly reduced the abundance of newly formed crystals, enlargement and aggregation of seeded crystals, and crystal adhesion on renal cell membranes. By contrast, E. coli at 1 × 10 CFU/ml significantly enhanced crystal growth and aggregation but did not affect crystallization and crystal-cell adhesion. Oxalate consumption assay showed that neither L. acidophilus nor E. coli significantly reduced the remaining oxalate level after 1 - 3 h incubation. However, both of them adhered to CaOx crystals. Surface component detection revealed that only L. acidophilus expressed S-layer protein, whereas only E. coli exhibited flagella on their surfaces. Removal of L. acidophilus S-layer protein and E. coli flagella completely abolished the inhibitory and promoting effects of L. acidophilus and E. coli, respectively.
L. acidophilus inhibits CaOx stone development by hampering crystallization, growth, aggregation and cell-adhesive ability of CaOx. By contrast, E. coli enhances CaOx stone development by promoting CaOx growth and aggregation. Their contradictory effects are most likely from differential surface components (i.e., S-layer protein on L. acidophilus and flagella on E. coli) not from oxalate-degrading ability. Video Abstract.
嗜酸乳杆菌是一种共生的尿路细菌，在健康个体中的丰度高于结石患者。因此，它被认为在肾结石病（KSD）中发挥抑制作用，但机制尚不清楚。因此，我们研究了嗜酸乳杆菌与已知促进草酸钙（CaOx）结石形成的大肠杆菌相比，对草酸钙结石形成的直接影响。
1×10 CFU/ml 的嗜酸乳杆菌显著减少了新形成晶体的丰度、 seeded 晶体的增大和聚集以及晶体对肾细胞膜的粘附。相比之下，1×10 CFU/ml 的大肠杆菌显著增强了晶体生长和聚集，但不影响结晶和晶体-细胞粘附。草酸盐消耗测定表明，在 1-3 小时孵育后，嗜酸乳杆菌和大肠杆菌均未显著降低剩余草酸盐水平。然而，它们都粘附在 CaOx 晶体上。表面成分检测表明，只有嗜酸乳杆菌表达 S-层蛋白，而只有大肠杆菌在其表面表现出鞭毛。去除嗜酸乳杆菌的 S-层蛋白和大肠杆菌的鞭毛完全消除了嗜酸乳杆菌和大肠杆菌的抑制和促进作用。
嗜酸乳杆菌通过阻碍 CaOx 的结晶、生长、聚集和细胞粘附能力来抑制 CaOx 结石的形成。相比之下，大肠杆菌通过促进 CaOx 的生长和聚集来增强 CaOx 结石的形成。它们的相反作用很可能来自于不同的表面成分（即嗜酸乳杆菌上的 S-层蛋白和大肠杆菌上的鞭毛），而不是草酸盐降解能力。
