Department of Microbiology and Immunology, Basic Medicine College, Jinan University, 510632 Guangzhou, Guangdong, China.
School of Chemistry & Pharmaceutical Sciences, Guangxi Normal University, 541001 Guilin, Guangxi, China.
Front Biosci (Landmark Ed). 2023 Mar 2;28(3):43. doi: 10.31083/j.fbl2803043.
Stability of intestinal flora is not only important for maintaining stable immune functions; it is also a key immune channel communicating the interaction between lung and intestine. In this study, probiotics and fecal microbiota transplantation (FMT) were used to regulate influenza-infected mice with antibiotic-induced intestinal dysbiosis and the effects of intestinal microorganisms on these mice were subsequently observed and evaluated.
Mice are housed in a normal environment with intranasal infection with influenza virus (FM1). Real-time quantitative polymerase chain reaction (RT-qPCR) was used to determine messenger RNA expression and lung viral replication of toll-like receptor 7 (TLR7), myeloid differentiation primary reaction 88 (MyD88) and nuclear factor κB (ss) p65 in the TLR7 signaling pathway. Western blotting is used to measure the expression levels of TLR7, MyD88, and NF-κB p65 proteins. Flow cytometry was used to detect the proportion of Th17/T regulated cells.
Results showed that compared with the simple virus group, both diversity and species of intestinal flora in influenza-infected mice with antibiotic-induced intestinal dysbiosis were lower, viral replication was significantly increased, lung and intestinal tissues were seriously damaged, degree of inflammation increased, expression of the TLR7 signaling pathway increased, and the Th1/Th2:Th17/Treg ratio decreased. Probiotics and FMT effectively regulated intestinal flora, improved pathological lung changes and inflammation caused by influenza infection, and adjusted the TLR7 signaling pathway and the Th1/Th2:Th17/Treg ratio. This effect was not obvious in TLR7-/- mice.In summary, by affecting the TLR7 signaling pathway, intestinal microorganisms reduced the inflammatory response in the lungs of influenza-infected mice with imbalances in antibiotic flora.
By affecting the TLR7 signaling pathway, intestinal microorganisms reduced the inflammatory response in the lungs of influenza-infected mice with imbalances in antibiotic flora. In summary, damage to lung tissue and intestinal mucosa in influenza-infected mice with antibiotic-induced intestinal dysbiosis is more serious compared to simple virus-infected mice. Improving intestinal flora using probiotics or FMT can alleviate intestinal inflammation and improve pulmonary inflammation through the TLR7 signaling pathway.
肠道菌群的稳定性不仅对于维持稳定的免疫功能非常重要，也是肺肠相互作用的关键免疫途径。本研究通过使用益生菌和粪便微生物移植（FMT）调节抗生素诱导的肠道菌群失调流感感染小鼠，并观察和评估肠道微生物对这些小鼠的影响。
将小鼠饲养在正常环境中，通过鼻腔内感染流感病毒（FM1）。采用实时定量聚合酶链反应（RT-qPCR）测定 Toll 样受体 7（TLR7）信号通路中 TLR7、髓样分化初级反应 88（MyD88）和核因子 κB（ss）p65 的信使 RNA 表达和肺病毒复制。Western blot 用于测量 TLR7、MyD88 和 NF-κB p65 蛋白的表达水平。流式细胞术用于检测 Th17/Treg 调节细胞的比例。
结果表明，与单纯病毒组相比，抗生素诱导的肠道菌群失调流感感染小鼠的肠道菌群多样性和种类均降低，病毒复制明显增加，肺和肠道组织严重受损，炎症程度增加，TLR7 信号通路表达增加，Th1/Th2：Th17/Treg 比值降低。益生菌和 FMT 可有效调节肠道菌群，改善流感感染引起的肺部病理变化和炎症，并调节 TLR7 信号通路和 Th1/Th2：Th17/Treg 比值。在 TLR7-/-小鼠中，这种作用并不明显。总之，肠道微生物通过影响 TLR7 信号通路，降低了抗生素菌群失衡流感感染小鼠肺部的炎症反应。
通过影响 TLR7 信号通路，肠道微生物降低了抗生素菌群失衡流感感染小鼠肺部的炎症反应。总之，与单纯病毒感染小鼠相比，抗生素诱导的肠道菌群失调流感感染小鼠的肺组织和肠道黏膜损伤更为严重。通过使用益生菌或 FMT 改善肠道菌群，可以通过 TLR7 信号通路减轻肠道炎症并改善肺部炎症。
