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| Correlation Analysis of Neonatal VAP Mice and Copeptin IL-32 IL-17 Levels and Different Degrees of Pneumonia |
| FANG Ping, WANG Ya, WU Di, et al |
| North Sichuan Medical College, Sichuan Nanchong 637100, China |
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Abstract Objective: To explore the symptoms and influencing factors of ventilator-associated pneumonia (VAP) to provide a basis for clinical diagnosis and treatment. Methods: 54 Balb/c mice were randomly divided into a control group, mild group (1×106 cfu/L), severe group (6×106 cfu/L) (n=18). Except for the control group, mice were mechanically ventilated for 24 hours and tracheal instillation of Pseudomonas aeruginosa to construct a VAP model. Forced vital capacity (FVC) and forced expiratory volume in the first second (FEV1) were measured at 1, 3, and 7 days after the model was constructed, respectively, and the value of FEV1/FVC% was calculated. The contents of Copeptin, IL-32 and IL-17 in serum were determined by ELISA. The staining was used to observe the histopathological changes of lung after 7 days. The protein expression levels of NF-κB, TLR2 and TLR4 in lung tissues were determined by immunohistochemical after 7 days. The lung function indexes were correlated with the levels of Copeptin, IL-32 and IL-17. The results of Copeptin, IL-32, IL-17 and the incidence of VAP were analyzed by ROC to evaluate the risk factors of VAP. Results: Within 7 days after the occurrence of VAP, compared with the control group, the FVC and FEV1 levels of the mild and severe groups were decreased, while the serum levels of Copeptin, IL-32 and IL-17 were increased (P<0.05); The number of inflammatory cells, neutrophils and the expression of TRL2, TRL4 and NF-κB protein in lung increased with the aggravation of VAP symptoms; Correlation analysis and ROC analysis showed that lung function indexes were closely correlated with the levels of Copeptin, IL-32, and IL-17, with a negative correlation trend. Conclusion: The incidence of ventilator-associated pneumonia is closely related to Copeptin, IL-32 and IL-17, and its mechanism may be related to the activation of NF-κB pathway to mediate inflammatory response, thereby reducing lung function.
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2021, Vol. 27 
