Zeng Wenjing, Zhang Qin, Feng Gang, Liu Gongliang, Wu Fenglin, Shen Han, Shao Hongwei, Tao Changli
Guangdong Province Key Laboratory for Biotechnology Drug Candidates, School of Biosciences and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
College of Light Industry and Food, Guangdong Provincial Key Laboratory of Lingnan Specialty Food Science and Technology, Zhongkai University of Agriculture and Engineering, Guangzhou, 510225, China.
Appl Microbiol Biotechnol. 2022 Apr;106(8):3265-3278. doi: 10.1007/s00253-022-11896-0. Epub 2022 Apr 4.
This study aimed to evaluate the effect of supplementation with inulin-type fructans (ITFs) on the intestinal immune function in the context of dysbiosis resulting from antibiotic cocktail (ABx) treatment. BALB/c mice (8-9 weeks of age) were treated with an ABx for 3 weeks and then allowed to recover spontaneously or with ITF supplementation (5%) for 4 weeks. Our results showed that ABx treatment can induce gut microbiota dysbiosis and intestinal inflammation in mice. After 4 weeks of recovery, ITF supplementation restored the composition of the intestinal microbial community. However, compared with spontaneous recovery, ITF supplementation delayed inflammation recovery in the intestine and upregulated diamine oxidase (DAO) activity and increased lipopolysaccharide (LPS) content in serum. In addition, ITF supplementation delayed the regulatory T (Treg) cell and B cell recovery in the lamina propria (LP). Furthermore, compared with spontaneous recovery, ITF supplementation inhibited the relative expression of certain proinflammatory genes, such as for inducible nitric oxide synthase (iNOS) and tumour necrosis factor α (Tnf-α), in the colon, but it reduced the secretion of the anti-inflammatory mediator transforming growth factor β1 (TGF-β1) in serum, reduced the secretion of secretory immunoglobulin A (SIgA) in the colon and promoted the secretion of the proinflammatory cytokine interleukin (IL)-17A. In conclusion, these data supported the hypothesis that the influence of ITFs on the host's intestinal status is not always beneficial in the context of ABx-induced biological disorder. However, the significance of these findings needs to be determined by advanced studies KEY POINTS: • ITFs did not promote the recovery of microbial community composition. • ITFs delayed the recovery of ABx-induced colonic inflammation. • ITFs reduced the secretion of TGF-β1 and SIgA. • ITFs delayed the recovery of Treg and B cells in the LP.
本研究旨在评估补充菊粉型果聚糖（ITFs）对抗生素联合治疗（ABx）导致的肠道菌群失调情况下肠道免疫功能的影响。选用8 - 9周龄的BALB/c小鼠，用ABx治疗3周，然后让其自行恢复或补充ITF（5%）4周。我们的结果表明，ABx治疗可诱导小鼠肠道微生物群失调和肠道炎症。恢复4周后，补充ITF恢复了肠道微生物群落的组成。然而，与自行恢复相比，补充ITF延迟了肠道炎症的恢复，上调了二胺氧化酶（DAO）活性，并增加了血清中脂多糖（LPS）的含量。此外，补充ITF延迟了固有层（LP）中调节性T（Treg）细胞和B细胞的恢复。此外，与自行恢复相比，补充ITF抑制了结肠中某些促炎基因的相对表达，如诱导型一氧化氮合酶（iNOS）和肿瘤坏死因子α（Tnf-α），但它降低了血清中抗炎介质转化生长因子β1（TGF-β1）的分泌，减少了结肠中分泌型免疫球蛋白A（SIgA）的分泌，并促进了促炎细胞因子白细胞介素（IL）-17A的分泌。总之，这些数据支持了以下假设：在ABx诱导的生物学紊乱情况下，ITFs对宿主肠道状态的影响并不总是有益的。然而，这些发现的意义需要通过进一步的研究来确定要点：• ITFs未促进微生物群落组成的恢复。• ITFs延迟了ABx诱导的结肠炎症的恢复。• ITFs减少了TGF-β1和SIgA的分泌。• ITFs延迟了LP中Treg和B细胞的恢复。
