Abstract

Previous studies mainly focused on the inflammatory responses caused by Mycoplasma gallisepticum (MG) in the chicken respiratory mucosa, setting the stage for chronic infection and disease manifestation. However, the underlying mechanism is still unknown. Spleen and thymus are important immune organs, which play a critical role in eliciting protective immune responses to ensure healing process and elimination of harmful stimuli. In the present study, the effects of MG infection on chicken spleen and thymus were investigated. The results showed that MG infection reduced antioxidant activities and induced oxidative stress in the spleen and thymus tissues. Histological examination showed normal morphology of chicken spleen and thymus in control group compared to MG infection group. In contrast, increased number of necrotic and nuclear debris, lymphocytolysis, prominent reticuloepithelial cells and loose arrangement of cells in the spleen and thymus were seen in MG-infected chickens. Ultrastructural analysis indicated nuclear and mitochondrial damage including mitochondrial swelling, deformation of nuclear membrane and congestion of chromatin material in MG infection group. The mRNA and protein expression of apoptosis-related genes were significantly upregulated in the spleen and thymus of MG-infected chickens compared to control group. Moreover, Terminal deoxynucleotidyl transferase–mediated dUTP nick endlabeling (TUNEL) assay results suggested that MG infection increased the number of positive-stained nuclei in the spleen and thymus. Meanwhile, the mRNA expression of mitochondrial dynamics in the spleen and thymus were altered by MG infection. In summary, these results showed that MG induced oxidative stress and apoptosis, which could be the possible causes associated with the immune damage, structural impairment and disease pathogenesis of MG infection.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.