The Expression Pattern of HSF1 and Its Regulating HSP70/TLR2 Expression during MO Infection

Mycoplasma ovipneumoniae (Mo) is a highly contagious pathogen that causes pneumonia in sheep, seriously threatening the sheep industry. Heat Shock Factor 1 (HSF1) is known to be important for host defense against lung infections, but its role in Mo infection was not understood. This study aimed to clarify HSF1 function during Mo infection. We created an in vivo infection model using Argali Hybrid Sheep and an in vitro model using alveolar macrophages. Immunohistochemistry was applied to check HSF1 expression and location in lung tissues. ELISA tests measured IL-6 and CXCL1 levels in serum and bronchoalveolar lavage fluid (BALF), while Western blot and RT-qPCR assessed HSF1, HSP70, and TLR2 expression in infected lungs and macrophages. Additionally, alveolar macrophages with overexpressed HSF1 were infected with Mo to study HSF1 regulation. Findings showed higher IL-6 and CXCL1 in BALF from infected sheep. Infected lung tissues and macrophages had lower HSF1 and HSP70 expression but higher TLR2 expression. Immunohistochemistry revealed less HSF1 in cell nuclei. Overexpressing HSF1 partly brought back HSP70 levels, reduced TLR2 increase, and improved Mo clearance. HSF1 overexpression enhances the immune response to Mo by controlling the HSP70/TLR2 pathway, offering a scientific foundation for strategies to prevent and control Mo infection.