Zhong Lemiao, Wu Chunlin, Liao Lvyan, Wu Yijian
University Key Laboratory for Integrated ChineseTraditional and Western Veterinary Medicine and Animal Healthcare, Fuzhou, Fujian Province, China.
Fujian Key Laboratory of Traditional Chinese Veterinary Medicine and Animal Health, Fujian Agriculture And Forestry University, Fuzhou, Fujian Province, China.
Virulence. 2023 Nov 14:2283895. doi: 10.1080/21505594.2023.2283895.
Mycoplasma synovium (MS) is a prominent avian pathogen known to elicit robust inflammatory responses in birds while evading immune detection, often leading to chronic infection and immune compromise. The mechanisms underpinning MS-mediated splenic tissue damage in chickens, however, remain undefined. In our investigation with 7-day-old SPF chickens, we administered an MS-Y bacterial solution (200 µl, 1 × 10 CCU/ml) through eye and nose droplets, collecting spleen samples on days 3, 6, and 12 post-infection. Comprehensive analyses utilizing histopathology, electron microscopy, TUNEL assay, qRT-PCR, and western blot were employed. Results demonstrated that MS-infection downregulated T-SOD, GSH-PX, and CAT, while concurrently elevating iNOS, NO, and MDA levels. Evidently, MS-induced oxidative stress compromised the spleen's antioxidant defences. Histological examinations pinpointed splenic damage characterized by lymphocyte reduction and increased inflammatory cell infiltration. Ultrastructural observations revealed clear apoptotic markers, including mitochondrial perturbations and nuclear anomalies. Importantly, MS induced significant spleen tissue apoptosis, as supported by TUNEL assay outputs and gene expression profiles associated with apoptosis. Concurrently, we observed upregulated expressions of mRNAs and proteins affiliated with the NF-κB/MAPK signalling cascade ( < 0.05). Collectively, our data elucidate that MS infection induces splenic apoptosis and oxidative disturbances, perturbs tissue integrity, and potentiates the NF-κB/MAPK-mediated inflammatory cascade.
滑膜支原体（MS）是一种重要的禽类病原体，已知它能在禽类中引发强烈的炎症反应，同时逃避免疫检测，常常导致慢性感染和免疫功能受损。然而，MS介导的鸡脾脏组织损伤的机制仍不明确。在我们对7日龄SPF鸡的研究中，我们通过眼鼻滴注给予MS-Y菌液（200 μl，1×10 CCU/ml），在感染后第3天、第6天和第12天采集脾脏样本。采用了组织病理学、电子显微镜、TUNEL检测、qRT-PCR和蛋白质印迹等综合分析方法。结果表明，MS感染下调了T-SOD、GSH-PX和CAT的水平，同时升高了iNOS、NO和MDA的水平。显然，MS诱导的氧化应激损害了脾脏的抗氧化防御能力。组织学检查发现脾脏损伤的特征是淋巴细胞减少和炎症细胞浸润增加。超微结构观察揭示了明显的凋亡标志物，包括线粒体紊乱和核异常。重要的是，TUNEL检测结果和与凋亡相关的基因表达谱支持了MS诱导显著的脾脏组织凋亡。同时，我们观察到与NF-κB/MAPK信号级联相关的mRNA和蛋白质表达上调（<0.05）。总体而言，我们的数据表明，MS感染诱导脾脏凋亡和氧化紊乱，扰乱组织完整性，并增强NF-κB/MAPK介导的炎症级联反应。
