Mycoplasma synoviae induce spleen tissue damage and inflammatory response of chicken through oxidative stress and apoptosis

滑液支原体通过氧化应激和细胞凋亡诱导鸡脾脏组织损伤和炎症反应。

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Abstract

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(9) 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 (p < 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.

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