■简介:流感病毒主要针对呼吸道,然而,在感染期间,呼吸系统和肠道系统都会受到损害。肺和肠损伤之间的联系仍不清楚。
■我们的实验采用16SrRNA技术和液相色谱-质谱(LC-MS)来检测流感病毒感染对小鼠粪便含量和代谢产物的影响。此外,通过HE染色研究流感病毒感染对肠道损伤的影响及其机制,蛋白质印迹,Q-PCR,和流式细胞术。
■我们的研究发现,流感病毒感染对肺部和肠道造成了重大损害,病毒只在肺部检测到。抗生素治疗加重了肺和肠损伤的严重程度。此外,感染后肺中Toll样受体7(TLR7)和干扰素-b(IFN-b)的mRNA水平显着增加。对肠道微生物群的分析显示,流感感染后成分发生了显着变化,包括增加的肠杆菌科和减少的乳杆菌科。相反,抗生素治疗减少了微生物多样性,特别是影响Firmicutes,变形杆菌,和拟杆菌。代谢组学显示由于流感感染和抗生素引起的氨基酸代谢途径的改变。吲哚胺2,3-双加氧酶1(IDO1)在结肠中的异常表达破坏了肠道中辅助T17细胞(Th17)和调节性T细胞(Treg细胞)之间的平衡。感染流感病毒并补充色氨酸和乳酸菌的小鼠显示出减少的肺和肠道损伤,肠杆菌在肠道中的水平降低,IDO1活性下降。
■总的来说,流感感染对肺和肠组织造成损害,肠道微生物群和代谢产物被破坏,影响Th17/Treg平衡。抗生素治疗加剧了这些影响。补充色氨酸和乳酸菌可改善肺部和肠道健康,强调对流感引起的肠道疾病中肺-肠连接的新认识。
UNASSIGNED: Introduction: The influenza virus primarily targets the respiratory tract, yet both the respiratory and intestinal systems suffer damage during infection. The connection between lung and intestinal damage remains unclear.
UNASSIGNED: Our experiment employs 16S rRNA technology and Liquid Chromatography-Mass Spectrometry (LC-MS) to detect the impact of influenza virus infection on the fecal content and metabolites in mice. Additionally, it investigates the effect of influenza virus infection on intestinal damage and its underlying mechanisms through HE staining, Western blot, Q-PCR, and flow cytometry.
UNASSIGNED: Our study found that influenza virus infection caused significant damage to both the lungs and intestines, with the virus detected exclusively in the lungs. Antibiotic treatment worsened the severity of lung and intestinal damage. Moreover, mRNA levels of Toll-like receptor 7 (TLR7) and Interferon-b (IFN-b) significantly increased in the lungs post-infection. Analysis of intestinal microbiota revealed notable shifts in composition after influenza infection, including increased Enterobacteriaceae and decreased Lactobacillaceae. Conversely, antibiotic treatment reduced microbial diversity, notably affecting Firmicutes, Proteobacteria, and Bacteroidetes. Metabolomics showed altered amino acid metabolism pathways due to influenza infection and antibiotics. Abnormal expression of indoleamine 2,3-dioxygenase 1 (IDO1) in the colon disrupted the balance between helper T17 cells (Th17) and regulatory T cells (Treg cells) in the intestine. Mice infected with the influenza virus and supplemented with tryptophan and Lactobacillus showed reduced lung and intestinal damage, decreased Enterobacteriaceae levels in the intestine, and decreased IDO1 activity.
UNASSIGNED: Overall, influenza infection caused damage to lung and intestinal tissues, disrupted intestinal microbiota and metabolites, and affected Th17/Treg balance. Antibiotic treatment exacerbated these effects. Supplementation with tryptophan and Lactobacillus improved lung and intestinal health, highlighting a new understanding of the lung-intestine connection in influenza-induced intestinal disease.