Abstract
Pseudomonas aeruginosa is a highly drug-resistant pathogen known to impair wound healing and provoke inflammatory responses, potentially leading to immune dysregulation. This study aimed to systematically investigate the immune response mechanisms mediated by cytokines following P. aeruginosa infection through the development of a standardized wound model. Kunming mice were selected as experimental subjects and given 8 mm diameter lesions on their backs and inoculated with standard strains PAO1 and PA14. The key parameters assessed included changes in body weight, wound redness and swelling, bacterial dynamics, protein content in wound tissues, immune responses, and pathological alterations. The results demonstrated that pathogen invasion significantly inhibited wound healing, with healing rates in the infected groups (87.5 ± 6.3% and 77.1 ± 3.6%) being notably lower than those in the uninfected control group. P. aeruginosa persisted in the wounds for up to 12 days, with bacterial loads decreasing from 8 log to 2 log. Additionally, there was a marked reduction in the protein content of the wound tissue and an increase in the expression levels of inflammatory factors such as IL-1β and TNF-α. The thickness of granulation tissue and the number of neovessels were significantly lower compared to the uninfected control group. This study establishes a standardized paradigm for creating a mouse model of P. aeruginosa infection in wounds, emphasizing the importance of appropriate mouse strains, uniform wound preparation methods, and moderate inoculation doses for reliable and accurate experimental results. These elements will facilitate the assessment of changes across six key indicators post-infection, providing a foundational data set and technical support for future mechanistic investigations of P. aeruginosa infection and the development of targeted antimicrobial strategies.