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.
方平, 王娅, 吴迪, 赵婧. 新生VAP小鼠和肽素 IL-32 IL-17水平变化与不同程度肺炎的相关性分析[J]. 河北医学, 2021, 27(9): 1409-1413.
FANG Ping, WANG Ya, WU Di, et al. Correlation Analysis of Neonatal VAP Mice and Copeptin IL-32 IL-17 Levels and Different Degrees of Pneumonia. HeBei Med, 2021, 27(9): 1409-1413.
[1] Pathak K V,Mcgilvrey M I,Hu C K,et al.Molecular profiling of innate immune response mechanisms in ventilator-associated pneumonia[J].Mol Cell Proteomics,2020,19(10):1688~1705. [2] 符媛,夏丽琼.新生儿呼吸机相关性肺炎危险因素分析[J].云南医药,2018,39(2):163~165. [3] Jorens P G.Sticking to an old definition of ventilator-associated pneumonia is not old-fashioned[J].Respir Care,2016,61(3):390~392. [4] De Winter F H R,S Jongers B,Bielen K,et al.Mechanical ventilation impairs IL-17 cytokine family expression in ventilator-associated pneumonia[J].Int Mol Sci,2019,20(20):5072. [5] Bielen K,S Jongers B,Boddaert J,et al.Mechanical ventilation induces interleukin 4 secretion in lungs and reduces the phagocytic capacity of lung macrophages[J].Infect Dis,2018,217(10):1645~1655. [6] Wienhold S M,Macrì M,Nouailles G,et al.Ventilator-induced lung injury is aggravated by antibiotic mediated microbiota depletion in mice[J].Crit Care,2018,22(1):282. [7] Winther J A,Brynildsen J,Hoiseth A D,et al.Prognostic and diagnostic significance of copeptin in acute exacerbation of chronic obstructive pulmonary disease and acute heart failure:data from the ACE 2 study[J].Respir Res,2017,18(1):184. [8] Song H W,Yang C,Liu W,et al.Interleukin-17A plays the same role on mice acute lung injury respectively induced by lipopolysaccharide and paraquat[J].Inflammation,2017,40(5):1509~1519. [9] Lee Y S,Kim K C,Mongre R K,et al.IL-32γ suppresses lung cancer stem cell growth via inhibition of ITGAV-mediated STAT5 pathway[J].Cell Death Dis,2019,10(7):506. [10] Alsaleh G,Sparsa L,Chatelus E,et al.Innate immunity triggers IL-32 expression by fibroblast-like synoviocytes in rheumatoid arthritis[J].Arthritis Res Ther,2010,12(4):135.
2021, Vol. 27 
冀公网安备13080202000677号