Transcriptomic Analysis of Lung Tissue in C57BL/6 Mice Infected with Beta Variant of SARS-CoV-2 and Experimental Validation of Chemokines
This study aimed to analyze the gene expression changes in the lungs of mice infected with Beta variant of SARS-CoV-2 at the transcriptomic level,in order to reveal the expression of mild pulmonary damage induced key host factors.First,a mouse model of C57BL/6 infected with Beta variant was established,and pathogen detection,histopathological analysis,and differential gene expression analysis were conducted on the lung tissues of mice infected and uninfected on the third day.Finally,five key genes involved in inflammatory responses that may contribute to lung damage were selected for validation using RT-qPCR.The results demonstrated that Beta variant effectively infected the lungs of C57BL/6 mice and led to mild pathological damage.In infected mice,Beta variant activated the innate immune responses in lung tissues,primarily including pathways such as Toll-like receptor signaling,type I and type Ⅱ interferon responses,leukocyte chemotaxis,and cytokine responses.By comparing the transcrip tomes of lung tissues between severe and mild infection in mice,inflammatory response chemokines associated with disease severity were identified,including Ccl2,Cc17,CxcI9,Cxcl10 and Cxcl14.RT-qPCR validation confirmed that the gene expression changes were consistent with the transcriptomic results,indicating that the excessive activation of these chemokines was associated with the degree of lung pathological damage.In summary,this study revealed that the infection of mice lungs by Beta variant activates key factors of the host inflammatory response pathway,which may be one of the main causes of mild pathological damage in mice lungs.This provides valuable research targets for the prevention and treatment of SARS-CoV-2 infection.
Beta variant of SARS-CoV-2Lung injuryInnate immunityInflammatory factorsTranscriptome
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