Study on the mechanism of Mycoplasma gallisepticum infection on chicken tracheal mucosa injury

Mycoplasma gallisepticum (MG) is a pathogenic microorganism that causes serious harm to the poultry industry. It is mainly adsorbed on the cilia and mucosa of respiratory epithelial cells, causing tracheal mucosal damage or cilia loss, resulting in chronic respiratory disease. In order to study the effect of MG infection on chicken tracheal mucosa injury and explore its possible mechanism, specific pathogen-free chickens were challenged with MG wild-type strain MG-HY. Then, transcriptome sequencing analysis was performed to study the mechanism of MG tracheal mucosal damage. During infection, MG localizes and proliferates in the chicken trachea, and induces mucosal damage. A total of 3112 significantly (P < 0.01) differentially expressed genes were selected by RNA-seq, including 1646 up-regulated genes and 1466 down-regulated genes. Functional analysis showed increased expression levels of genes involved in the immune defense response and the mechanical barrier of the tracheal mucosa in infected chicks. The expression level of pro-inflammatory cytokines (TNF-α) increased, activating the upstream protein Ras of the extracellular signal regulated protein kinase (ERK)-myosin light chain kinase (MLCK) signalling pathway, causing ERK phosphorylation levels to rise and MLCK activation. This causes phosphorylation of myosin light chain, and further regulating the expression and mucous distribution of tight junction protein, leading to tracheal mucosal injury in chicks. The results of qRT-PCR assay and immunohistochemical analysis were consistent with the results of transcriptome analysis. Overall, our findings provide a basis for further research on the underlying mechanism of chick tracheal mucosal damage caused by MG infection, and help to understand how MG induces respiratory immune damage in birds. RESEARCH HIGHLIGHTSMG infection causes a persistent inflammatory response by increasing the expression of immune response genes. The ERK-MLCK signalling pathway activated by MG infection regulates tight junction proteins in the tracheal mucosa. These data provide a basis for future prevention and treatment studies to control MG infection.