MOE Joint International Research Laboratory of Animal Health and Food Safety, Key Laboratory of Animal Bacteriology, Ministry of Agriculture, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
College of Veterinary Medicine, Jilin Provincial Engineering Research Center of Animal Probiotics, Jilin Provincial Key Laboratory of Animal Microecology and Healthy Breeding, Engineering Research Center of Microecological Vaccines (Drugs) for Major Animal Diseases, Ministry of Education, Jilin Agricultural University, Changchun, China.
mSystems. 2024 Aug 20;9(8):e0050124. doi: 10.1128/msystems.00501-24. Epub 2024 Jul 25.
Infection with precipitates a spectrum of pathologies in bovines, notably necrotic pneumonia, mastitis, and arthritis, impinging upon the health and nutritional assimilation of these animals. A pivotal factor, lipocalin 2 (Lcn2), is responsive to microbial invasion, inflammatory processes, and tissue damage, the extent of which Lcn2 modulates the gut environment, however, remains unclear in response to -induced alterations. To explore the role of Lcn2 in shaping the gut milieu of mice during a 5-week period post infection, Lcn2 knockout Lcn2 mice were scrutinized for changes in the gut microbiota and metabolomic profiles. Results showed that Lcn2 mice infected with exhibited notable shifts in the operational taxonomic units (OTUs) of gut microbiota, alongside significant disparities in α and β diversity. Concomitantly, a marked increase was observed during the 5-week period in the abundance of Akkermansia, Oscillospira, and Bacteroides, coupled with a substantial decrease in Ruminococcus within the microbiome of Lcn2 knockout mice. Notably, was significantly enriched in the gut flora of Lcn2 mice. Furthermore, the absence of Lcn2 significantly altered the gut metabolomic landscape, evidenced by elevated levels of metabolites such as taurodeoxycholic acid, 10-undecenoic acid, azelaic acid, and dodecanedioic acid in Lcn2 mice. Our findings demonstrated that the lack of Lcn2 in the context of infection profoundly affected the regulation of gut microbiota and metabolomic components, culminating in a transformed gut environment. Our results revealed that Lcn2 may regulate gut microbiota and metabolome components, changing the intestinal environment, thereby affecting the infection status of .
Our study addresses the critical knowledge gap regarding the specific influence of lipocalin 2 (LCN2) in the context of infection, particularly focusing on its role in the gut environment. Utilizing LCN2 knockout (Lcn2) mice, we meticulously assessed changes in the gut microbiota and metabolic components following infection. Our findings reveal alterations in the gut microbial community, emphasizing the potentially crucial role of LCN2 in maintaining stability. Furthermore, we observed significant shifts in specific microbial communities, including the enrichment of , known for its positive impact on intestinal health and immune regulation. The implications of our study extend beyond understanding the dynamics of the gut microbiome, offering insights into the potential therapeutic strategies for gut-related health conditions and microbial dysbiosis.
感染 可引发牛群一系列病理学变化，特别是坏死性肺炎、乳腺炎和关节炎，影响这些动物的健康和营养吸收。一个关键因素是脂钙蛋白 2（Lcn2），它对微生物入侵、炎症过程和组织损伤有反应，但在应对 引起的改变时，Lcn2 调节肠道环境的程度尚不清楚。为了研究 Lcn2 在感染后 5 周内塑造感染小鼠肠道环境的作用，研究人员仔细观察了 Lcn2 敲除（Lcn2）小鼠的肠道微生物群和代谢组学特征的变化。结果表明，感染 的 Lcn2 小鼠的肠道微生物群的操作分类单位（OTUs）发生了显著变化，同时α和β多样性也存在显著差异。同时，在 5 周的时间内，Lcn2 敲除小鼠的微生物群中阿克曼氏菌、 Oscillospira 和拟杆菌的丰度显著增加，而 Ruminococcus 的丰度显著减少。值得注意的是， 在 Lcn2 小鼠的肠道菌群中显著富集。此外，Lcn2 的缺失显著改变了肠道代谢组学图谱，Lcn2 小鼠的 taurodeoxycholic 酸、10-十一烯酸、壬二酸和十二烷二酸等代谢物水平升高。我们的研究结果表明，在 感染的情况下，Lcn2 的缺失会显著影响肠道微生物群和代谢组学成分的调节，导致肠道环境发生变化。我们的研究结果表明，Lcn2 可能调节肠道微生物群和代谢组学成分，改变肠道环境，从而影响 的感染状态。
我们的研究解决了关于脂钙蛋白 2（LCN2）在 感染背景下的具体影响的关键知识空白，特别是关注其在肠道环境中的作用。我们利用 LCN2 敲除（Lcn2）小鼠，仔细评估了 感染后肠道微生物群和代谢成分的变化。我们的研究结果显示，肠道微生物群落发生了变化，这强调了 LCN2 在维持稳定性方面的潜在关键作用。此外，我们观察到特定微生物群落的显著变化，包括 的富集， 已知对肠道健康和免疫调节有积极影响。我们研究的意义不仅在于了解肠道微生物组的动态，还为肠道相关健康状况和微生物失调的潜在治疗策略提供了新的见解。
