School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Guangdong Provincial Key Laboratory of Microbial Safety and Health, State Key Laboratory of Applied Microbiology Southern China, Institute of Microbiology, Guangdong Academy of Sciences, Guangzhou, China.
Front Immunol. 2022 Sep 22;13:931871. doi: 10.3389/fimmu.2022.931871. eCollection 2022.
has attracted considerable attention due to its association with meningitis and necrotizing enterocolitis (NEC) in newborns. Generally, lipopolysaccharide (LPS) facilitates bacterial translocation along with inflammatory responses as an endotoxin; however, the pathogenicity of LPS and the strategies to alleviate the toxicity were largely unknown. In this study, inflammatory responses were stimulated by intraperitoneal injection of LPS into Sprague-Dawley young rats. Simultaneously, NCTC9343 were continuously fed through gavage for 5 days before or after injection of LPS to evaluate the intervention effect of . We first checked the morphological changes of the ileum and colon and the intestinal microbiota and then detected the generation of inflammatory factors, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10) and the expression of Toll-like receptor 4 (TLR4), occludin, claudin-4, and iNOs. The results indicated that . LPS exacerbated intestinal infection by altering gut microbe profile, tight junction protein expression, and releasing inflammatory factors in a time- and dose-dependent manner. Intriguingly, treatment with obviously diminished the pathological injuries and expression of TLR4 caused by LPS while increasing gut microbes like -9. We note that , , and might be positively related to . LPS infection, but -9 was negatively correlated. The results suggested that the intestinal microbiota is an important target for the prevention and treatment of pathogenic injuries induced by LPS.
由于其与新生儿脑膜炎和坏死性小肠结肠炎（NEC）的关联，它引起了相当多的关注。通常，脂多糖（LPS）作为内毒素促进细菌易位和炎症反应；然而，LPS 的致病性和减轻其毒性的策略在很大程度上是未知的。在这项研究中，通过向 Sprague-Dawley 幼鼠腹腔内注射 LPS 来刺激炎症反应。同时，在 LPS 注射前后通过灌胃连续喂养 NCTC93435 天，以评估 的干预效果。我们首先检查了回肠和结肠的形态变化以及肠道微生物群，然后检测了炎症因子的产生，包括肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）和白细胞介素-10（IL-10）以及 Toll 样受体 4（TLR4）、闭合蛋白、紧密连接蛋白 4 和 iNOS 的表达。结果表明，LPS 通过改变肠道微生物群谱、紧密连接蛋白表达和释放炎症因子，以时间和剂量依赖的方式加剧了肠道感染。有趣的是，用 明显减轻了 LPS 引起的病理损伤和 TLR4 的表达，同时增加了肠道微生物如 -9。我们注意到，、和 可能与 LPS 感染呈正相关，但 -9 呈负相关。结果表明，肠道微生物群是预防和治疗 LPS 引起的致病性损伤的重要靶点。
