化脓性Trueperella可引起猪严重的肺部疾病，但其发病机制尚不清楚。化脓性密螺旋体对猪支气管上皮细胞（PBEC）、猪精密切割肺切片（PCLS）和小鼠呼吸道上皮细胞造成的损害仍不清楚。在本研究中，我们使用化脓性密螺旋体 20121 在气液界面条件和猪 PCLS 中感染 PBEC。化脓性密螺旋体可以粘附、定植，并对 PCLS 中的 PBEC 和支气管管腔表面产生细胞毒性作用，从而损伤细支气管上皮。此外，受感染小鼠肺部的细支气管上皮细胞显示出广泛的变性。此外，蛋白质印迹显示NOD样受体（NLR）/C末端caspase募集结构域（ASC）/caspase-1轴和核因子-kappa B通路参与PCLS和小鼠肺部的炎症，这也证实了猪 PCLS 提供了一个分析肺部免疫反应的平台。同时，p-c-Jun N末端激酶、p-细胞外信号调节激酶和p-蛋白激酶B（AKT）的水平显着升高，这表明丝裂原激活蛋白激酶和Akt通路也参与炎症。在化脓性密螺旋体感染的小鼠中。此外，我们使用化脓性密螺旋体20121感染肿瘤坏死因子-α（tnf-α-/-）小鼠，结果表明感染的tnf-α-/-小鼠呼吸道上皮细胞凋亡和损伤减轻。因此，促炎细胞因子TNF-α在小鼠肺部细胞凋亡和呼吸道上皮损伤中发挥作用。总而言之，我们的研究深入了解了化脓性密螺旋体引起的炎症损伤，并表明阻断 NLR 可能是对抗化脓性密螺旋体感染的潜在治疗策略。

Trueperella pyogenes can cause severe pulmonary disease in swine, but the mechanism of pathogenesis is not well defined. T. pyogenes-induced damage to porcine bronchial epithelial cells (PBECs), porcine precision-cut lung slices (PCLS), and respiratory epithelium of mice remains unknown. In this study, we used T. pyogenes 20121 to infect PBECs in air-liquid interface conditions and porcine PCLS. T. pyogenes could adhere to, colonize, and induce cytotoxic effect on PBECs and the luminal surface of bronchi in PCLS, which damaged the bronchiolar epithelium. Moreover, bronchiolar epithelial cells showed extensive degeneration in the lungs of infected mice. Furthermore, western blot showed that the NOD-like receptor (NLR)/C-terminal caspase recruitment domain (ASC)/caspase-1 axis and nuclear factor-kappa B pathway were involved in inflammation in PCLS and lungs of mice, which also confirms that porcine PCLS provide a platform to analyze the pulmonary immune response. Meanwhile, the levels of p-c-Jun N-terminal kinase, p-extracellular signal-regulated kinase, and p-protein kinase B (AKT) were increased significantly, which indicated the mitogen-activated protein kinase and Akt pathways were also involved in inflammation in T. pyogenes-infected mice. In addition, we used T. pyogenes 20121 to infect tumor necrosis factor-alpha (tnf-α-/-) mice, and the results indicated that apoptosis and injury in respiratory epithelium of infected tnf-α-/- mice were alleviated. Thus, the pro-inflammatory cytokine TNF-α played a role in apoptosis and the respiratory epithelium injury in mouse lungs. Collectively, our study provides insight into the inflammatory injury induced by T. pyogenes and suggests that blocking NLR may be a potential therapeutic strategy against T. pyogenes infection.