Abstract
Mycoplasma bovis is one of the most important pathogens in animal husbandry, and the current infection and morbidity rates are increasing year by year, causing great losses to the farming industry and seriously affecting animal welfare. In this study, we took tracheal tissues from calves infected with M. bovis to make pathological tissue sections for observation, and selected tracheal tissues for transcriptome sequencing to screen differentially expressed genes based on the threshold |log2FoldChange| > 1 and Padjust < 0.05 and functional enrichment, to explore in depth the potential mechanisms of bovine tracheal damage caused by bovine tracheitis. Experiments were conducted to observe the changes in tracheal tissues after M. bovis infection through pathological sections of the trachea of M. bovis-infected calves. From the transcriptome sequencing results, we mined the main differential genes and important metabolic pathways of M. bovis causing damage to the trachea of calves. It was found that the cricoid cartilage tissue of the trachea was congested and hemorrhagic after M. bovis infection in calves, and the pathological sections showed localized necrosis of epithelial cells, disorganization, high inflammatory cell infiltration in the interepithelial and lamina propria, and some epithelial cell detachment. Transcriptome sequencing identified 4199 DEGs, including 1378 up-regulated genes and 2821 down-regulated genes. KEGG enrichment analysis indicated that the differential genes were enriched to 59 significantly differing signaling pathways, and a number of important metabolic pathways related to tracheitis induced by M. bovis-infected calves were unearthed. The major ones included IL-17, the Toll-like receptor, JAK/STAT, the PI3K-Akt signaling pathway, etc. In this study, we found that M. bovis infection of calves caused inflammatory damage to the trachea, and transcriptome sequencing results also showed significant differences in the expression of key genes such as IL-6 inflammatory factor, CASP8, and APOA1.