Expression And Significance Of IL-17A In The Lungs Of Mice Infected With Pseudomonas Aeruginosa

Objective: To observe Pseudomonas aeruginosa lung infection in amouse model of IL-17A expression, to analyze the role of IL-17A inPseudomonas aeruginosa lung infection in mice infected withPseudomonas aeruginosa lung treatment to find a new way. Methods:Thirty SPF Kunming white female mice,8-12weeks old, weighing17-23g, were randomly divided into control group and model group (n=15),model group drops from the mouse trachea into the configured0.03mlPseudomonas aeruginosa suspension control group from the mousetracheal instillation of the same volume of normal saline, the two groupsof mice in turns were killed by collected heart blood when the modelwere builded3h,9h,24h,5mice each time. Took the lung tissue in miceto do histopathologic slide and observated alveolar inflammation throughHE staining, detected expression of IL-6, IL-17A in serum of the mice byELISA and expression of IL-17A in the lung tissue throughimmunohistochemical. Results:(1)observed under HE staining lightmicroscopy: the control group: at all time points, the lung tissue structurewas clear and the alveolar structure was complete, there was no broken ordamaged alveolar walls, the alveolar cavity size and the alveolar intervalwas normal, also there was no inflammatory cell invasion and fibroustissue hyperplasia. Model group: At the third hour, the lung tissue structure was clear and the alveolar structure was complete, the alveolarwalls were not broken or damaged, and the alveolar cavity size wasnormal, there was a small amount of inflammatory cells invasion, thealveolar interval slightly thickened; At the ninth hour, the lung tissuestructure was clear but the alveolar structure was incomplete, the alveolarwalls were broken and damaged, part of the alveolar lumen was narrowedwith more inflammatory cells invaded,also the alveolar interval thickened;At the24th hour, the lung tissue structure was not clear and part of thealveolar walls structure was damaged, the alveolar walls obviouslythickened with a large number of inflammatory cells invasion,the alveolarlumen narrowed considerably or even disappeared with a large number ofred blood cells and inflammatory cells in it.(2) Immunohistochemical ofIL-17A in the lung tissue: At each time point, expression of IL-17A inthe lung tissue of the model group was higher than that of the controlgroup, and the difference was statistically significant (P <0.05). Expresionof IL-17A in the lung tissue of the Control group have no obviouschange at any time points,while expresion of IL-17A in the lung tissueof the experimental group increased over time.(3) serum IL-6and IL-17changes: Each time point serum IL-6concentration in model group werehigher than the control group, the difference was statistically significant(P <0.05);3hours after the model were builded,the expression of IL-17A in mice serum had no significant difference between the controlgroup and experimental group (P>0.05), while9hours and24hours after the model were builded, the expression of IL-17A in mice serumwere significantly higher than that of control group, the difference wasstatistically significant (P <0.05). There was no obvious change on theexpression of IL-6, IL-17A in mice serum of the Control group at anytime points while the expression of IL-6, IL-17A in mice serum ofmodel group increased over time.(4) serum IL-6and IL-17A into apositive correlation of serum IL-17A and alveolitis integral a positivecorrelation was statistically significant (P <0.05). Conclusion: IL-17Amay be through the recruitment of inflammatory cells involved in theinflammatory response and early pathogen Pseudomonas aeruginosa lunginfection removal process.