Gut-lung axis injury is a common finding in patients with respiratory diseases as well as in animal model of influenza virus infection. Influenza virus damages the intestinal microecology while affecting the lungs. Rifaximin, a non-absorbable derivative of rifamycin, is an effective antibiotic that acts by inhibiting bacterial RNA synthesis. This study aimed to determine whether rifaximin-perturbation of the intestinal microbiome leads to protective effects against influenza infection, via the gut-lung axis. Our results showed that influenza virus infection caused inflammation of and damage to the lungs. The expression of tight junction proteins in the lung and colon of H1N1 infected mice decreased significantly, attesting that the barrier structure of the lung and colon was damaged. Due to this perturbation in the gut-lung axis, the intestinal microbiota became imbalanced as Escherichia coli bacteria replicated opportunistically, causing intestinal injury. When influenza infection was treated with rifamixin, qPCR results from the gut showed significant increases in Lactobacillus and Bifidobacterium populations, while Escherichia coli populations markedly decreased. Furthermore, pathology sections and western blotting results illustrated that rifaximin treatment strengthened the physical barriers of the lung-gut axis through increased expression of tight junction protein in the colon and lungs. These results indicated that rifaximin ameliorated lung and intestine injury induced by influenza virus infection. The mechanisms identified were the regulation of gut flora balance and intestinal and lung permeability, which might be related to the regulation of the gut-lung axis. Rifaximin might be useful as a co-treatment drug for the prevention of influenza virus infection.

肠道肺轴损伤是呼吸系统疾病患者以及流感病毒感染动物模型中的常见发现。流感病毒在影响肺部的同时会损害肠道微生态。利福昔明是利福霉素的不可吸收衍生物，是一种有效的抗生素，可通过抑制细菌RNA合成发挥作用。这项研究旨在确定肠胃微生物组的利福昔明摄动是否会通过肠肺轴导致对流感感染的保护作用。我们的结果表明，流感病毒感染引起了肺部炎症和损害。H1N1感染小鼠的肺和结肠中紧密连接蛋白的表达显着下降，证明肺和结肠的屏障结构受到破坏。由于肠肺轴的这种扰动，大肠杆菌细菌是机会性复制的，引起肠道损伤。用利福米新治疗流感病毒感染后，肠道的qPCR结果显示乳杆菌和双歧杆菌种群显着增加，而大肠杆菌人口明显减少。此外，病理切片和蛋白质印迹结果表明，利福昔明治疗通过增加结肠和肺中紧密连接蛋白的表达来增强肺肠轴的物理屏障。这些结果表明利福昔明改善了由流感病毒感染引起的肺和肠损伤。确定的机制是调节肠道菌群平衡以及肠和肺通透性，这可能与调节肠肺轴有关。利福昔明可能用作预防流感病毒感染的辅助治疗药物。