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| 2021-11-17 11:58:45 | onclick： | The study revealed its immunopathological mechanism |
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China Academy of Sciences animal novel coronavirus pneumonia website 16 reported that the team found that the new crown pneumonia elderly macaque model delayed inflammatory response to the immune mechanism of the pathogenesis of Kunming. Relevant research results were recently published in the journal signal transmission and targeted therapy.
The novel coronavirus pneumonia is one of the main pathogenesis of the new crown pneumonia. The strong inflammatory reaction and cytokine storm cause severe damage to the lungs and other organs, including diffuse alveolar damage, micro thrombosis and multiple organ failure. Understanding the novel coronavirus pneumonia in the process of immunological characteristics is of great significance for its prevention and treatment. Primates animal models novel coronavirus pneumonia.
Previously, the research group of Zheng Yongtang, a researcher at the Kunming Institute of animal science, China Academy of Sciences, found that COVID-19 (SARS-CoV-2) infected China macaques showed similar pathological features to human patients. However, different from the characteristics of rapid immune response and timely decline of inflammatory response in young rhesus monkeys, old rhesus monkeys showed abnormal changes of delayed outbreak of inflammatory response in lung tissue. Researchers hypothesized that age related abnormal immune microenvironment may have been formed in the early stages of COVID-19 infection and continue to affect disease progression in elderly patients. Novel coronavirus pneumonia models in China were studied by more accurate immuno pathological studies based on paraffin sections and multiple immunofluorescence staining and IHC-FACS in situ quantitative analysis to test this hypothesis. Zheng Yongtang's team was based on paraffin sections.
By analyzing the non diseased lung tissue in the early stage of infection, the research team found that the virus infection was not significantly affected by age, and the ACE2 + cells in the lung tissue of old and young monkeys decreased significantly after infection. However, the apoptosis, autophagy and NF of ACE2 + cells in elderly rhesus monkeys- κ The level of B activation was more severe than that of young macaques.
In addition, inflammatory factors IFN- in lung tissue of old rhesus monkeys infected with COVID-19 α- And IL-6 secreting cells increased significantly, which provided the basis for the outbreak of inflammation after tissue lesions. Some cytokines and interferon signal proteins such as IFN are naturally highly expressed in the lung tissue of elderly rhesus monkeys- γ、 TNF- α And MX1, this immune tolerance caused by inflammatory aging passivates the response ability of the immune system and explains the delayed inflammatory response of the elderly macaque model. COVID-19 infection specifically induces the aggregation of CXCR3+ cells in the lung, spleen and peripheral blood of aged macaque monkeys, which is an age-related systemic pathological feature. Novel coronavirus pneumonia in COVID-19 infected with T-bet has a rapid decline in PBMC and CD8+ cells. The CXCR3+/T-bet+ ratio in CD8+ cells may be a good indicator for predicting the severity of new crown pneumonia. Only the increased expression of CXCR3 and the insufficient expression of T-bet may not be conducive to the normal antiviral effect of CD8 + cells. On the contrary, due to the compensatory effect, a large number of CXCR3 + cells are chemotactic to the infected site to promote inflammation, which may be one of the more serious mechanisms of pulmonary lesions in elderly macaques. (end)
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