Dong Yao, Han Mei, Qi Yongmei, Wu Ying, Zhou Zhipeng, Jiang Dacheng, Gai Zhonghui
Department of Research and Development, Wecare Probiotics Co., Ltd., Suzhou, China.
Department of Food Quality and Safety, Shanghai Business School, Shanghai, China.
Front Immunol. 2025 Jan 17;15:1469885. doi: 10.3389/fimmu.2024.1469885. eCollection 2024.
This study aimed to assess the impact of Lp05 (Lp05) on the gastrointestinal microbiome and pathophysiological status of mice infected with (), exploring its potential as a probiotic treatment for infections.
, the interaction between Lp05 and was analyzed using laser confocal and scanning electron microscopy. , C57BL/6 mice infected with were treated with Lp05 and divided into six groups: control, model, quadruple therapy, and three dosage levels of Lp05 (2×10, 2×10, 2×10 CFU/mouse/day). Over six weeks, the impact of Lp05 on the gastrointestinal microbiome and physiological markers was assessed. Measurements included digestive enzymes (α-amylase, pepsin, cellulase), inflammatory markers (interleukin-17A, interleukin-23, interleukin-10, interferon-β, interferon-γ, FoxP3, endothelin, IP-10, TGF-β1), oxidative stress markers (catalase, malondialdehyde, superoxide dismutase, myeloperoxidase), and tissue pathology (via modified Warthin-Starry silver and H&E staining). Microbial community structure in the stomach and intestines was evaluated through 16S rRNA gene sequencing.
studies showed Lp05 and formed co-aggregates, with Lp05 potentially disrupting cell structure, reducing its stomach colonization. , Lp05 significantly lowered gastric mucosal urease activity and serum -IgG antibody levels in infected mice ( < 0.01). It also mitigated pathological changes in the stomach and duodenum, decreased inflammatory responses (ET, IL-17A, IL-23, TGF-beta1, and IP-10, < 0.01 for all), and enhanced antioxidant enzyme activities (CAT and SOD, < 0.01) while reducing MDA and MPO levels ( < 0.01), combating oxidative stress from infection. Lp05 treatment significantly modified the intestinal and gastric microbiota, increasing beneficial bacteria like and , and decreasing harmful bacteria such as , linked to pathological conditions.
Lp05 effectively modulates the gastrointestinal microbiome, reduces inflammation and oxidative stress, and suppresses , promising for probiotic therapies with further research needed to refine its clinical use.
本研究旨在评估Lp05对感染（）小鼠胃肠道微生物群和病理生理状态的影响，探索其作为益生菌治疗感染的潜力。
使用激光共聚焦显微镜和扫描电子显微镜分析Lp05与（）之间的相互作用。将感染（）的C57BL/6小鼠用Lp05处理，并分为六组：对照组、模型组、四联疗法组以及三个Lp05剂量水平组（2×10、2×10、2×10 CFU/小鼠/天）。在六周时间内，评估Lp05对胃肠道微生物群和生理指标的影响。测量指标包括消化酶（α-淀粉酶、胃蛋白酶、纤维素酶）、炎症标志物（白细胞介素-17A、白细胞介素-23、白细胞介素-10、干扰素-β、干扰素-γ、叉头框蛋白3、内皮素、IP-10、转化生长因子-β1）、氧化应激标志物（过氧化氢酶、丙二醛、超氧化物歧化酶、髓过氧化物酶）以及组织病理学（通过改良的Warthin-Starry银染和苏木精-伊红染色）。通过16S rRNA基因测序评估胃和肠道中的微生物群落结构。
研究表明Lp05与（）形成共聚物，Lp05可能破坏（）细胞结构，减少其在胃中的定植。此外，Lp05显著降低感染小鼠的胃黏膜尿素酶活性和血清-IgG抗体水平（<0.01）。它还减轻了胃和十二指肠的病理变化，降低炎症反应（内皮素、白细胞介素-17A、白细胞介素-23、转化生长因子-β1和IP-10，所有均<0.01），增强抗氧化酶活性（过氧化氢酶和超氧化物歧化酶，<0.01），同时降低丙二醛和髓过氧化物酶水平（<0.01），对抗感染引起的氧化应激。Lp05治疗显著改变了肠道和胃微生物群，增加了有益菌如（）和（），减少了与病理状况相关的有害菌如（）。
Lp05有效调节胃肠道微生物群，减轻炎症和氧化应激，并抑制（），有望用于益生菌治疗，但需要进一步研究以完善其临床应用。
