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The Effect and Mechanism of Inhaled Glucocorticoids on Antibacterial Host Defense in An Asthmatic Mouse Model

Author: WangPeng
Tutor: LiGuoPing
School: Luzhou Medical College
Course: Internal Medicine
Keywords: Glucocorticoid Mice Asthma Host defense CRAMP
CLC: R562.25
Type: Master's thesis
Year: 2011
Downloads: 25
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Abstract

Objective: glucocorticoid is widely used in the most effective drug in the treatment of asthma, inhaled glucocorticoids are still the main control airway inflammation in asthma treatment, but asthma patients using inhaled corticosteroids host bacterium defense coverage less. The experimental asthma murine model of inhaled corticosteroids, airway, to P. aeruginosa nasal inhalation, inhaled corticosteroids in asthma host bacterial defense, and to explore its mechanism. Methods: 50 6-7 Zhou Jiankang female BALB / c mice were randomly divided into a control group, asthma group, asthma infection group, inhaled budesonide group, budesonide inhalation infection group, n = 10. Mice sensitized and challenged with ovalbumin (Ovalbumin, OVA) solution, the control group, only intraperitoneal injection of the same dose of saline. Followed by nebulized budesonide and infected with the 3 × 105CFU P. aeruginosa. After 24 hours, mice were sacrificed, and the collection and separation of serum and remove lung tissue. Lung tissue homogenate bacterial culture for bacteria and quantitative. The lung tissue HE staining of lung tissue inflammatory cell infiltration degree of histopathological changes in lung inflammation rated standard rules score (score of 1-4). The immunohistochemistry assay airway epithelial cells CRAMP expression levels. Immune Western blotting (Western Blot) semi-quantitative determination of CRAMP expression levels in lung tissue. ELISA assay of IL-4 and IFN-γ expression in peripheral blood serum. Results: 1. Mice general observation: the asthmatic mice gradually irritability, increased nasal secretions, flexible nose, shortness of breath and hair bleak, bristle symptoms. After the excitation of the budesonide group performance is significantly reduced compared with the asthma group. 24 hours after Pseudomonas aeruginosa infection, asthma, infections appear to move slowly, eyes closed, curled a mass and an increase in nasal secretions, the ear thermometer cold, such as performance. In addition to the above performance, budesonide infection group performance significantly chills, the mice get together and squeeze in a decreased appetite. 2. Changes in lung tissue endoscopic airway inflammation: asthma mice bronchial and alveolar space narrowing, widening of the alveolar septa, bronchial wall visible pulmonary interstitial inflammatory cell infiltration, mainly eosinophils, bronchial bronchioles and alveolar spaces visible exudate, the tracheal epithelial edema injury, partial necrosis shedding, with goblet cell hyperplasia. Inhaled budesonide group airway inflammation was significantly lighter than the asthma group around the airway inflammation is significantly reduced after drug treatment. Pseudomonas aeruginosa infection in 24 hours after infection group of asthma bronchial and alveolar space narrowing, part alveolar completely reduced, widened alveolar septum, bronchial wall and lung interstitial visible inflammatory cell infiltration, mainly eosinophils, bronchial bronchioles and alveolar space visible to a large number of exudate, the tracheal mucosa part of necrotic, with goblet cell hyperplasia. The inhaled budesonide infection group bronchial and alveolar space was significantly reduced, bronchioles and alveolar space completely disappeared, bronchial and alveolar spaces visible wide range of large number of exudate, the tracheal mucosa part of necrotic, visible pus. Lung tissue inflammation score: 0.01, budesonide infection group with asthma infection compared inflammatory asthma group compared with the control group inflammation invasion the apparent Cp lt; 0.01 in the budesonide group compared with asthma inflammation reduce ap lt; invasion obvious bp lt; 0.01 statistically meaningful. Lung bacterial quantitative: the number of bacterial colonies budesonide infection group was significantly higher than that asthma infection group, the difference between the two is significant P lt; 0.05 4. Lung CRAMP expression levels: Immunohistochemical detection of lung tissue CRAMP expression levels results found the budesonide group of antimicrobial peptides infected expression levels were significantly lower than asthma infection group. Immunoblot detection of lung tissue CRAMP expression levels results show that budesonide infection group striped gray value significantly reduced infection group than asthma, and each group was analyzed by Quantity One software gray value, budesonide infection group with asthma infection group phase significant than differences (P lt; 0.05). Mouse peripheral blood serum IL-4 and IFN-y level of determination: asthma group level of IL-4 and the control group was significantly increased (P lt; 0.01), IFN-y levels were significantly lower (P lt; 0.01). Budesonide group and IL-4 levels below the asthma group (P lt; 0.01), but the level of IFN-y was no significant difference between the two groups (P gt; 0.05). IL-4 levels of asthma infection group and the control group was significantly higher (P lt; 0.01), IFN-γ levels were significantly lower (P lt; 0.01). Budesonide infection of IL-4 levels higher than asthma infection group (P lt; 0.01), and IFN-γ levels lower than asthma infection group, the difference between the two groups was statistically significant (P lt; 0.01). Conclusion: The the asthmatic mice serum IL-4 levels significantly increased, decreased the level of IFN-γ, confirmed the Thl/Th2 of imbalance plays an important role in the pathogenesis of asthma. Inhaled budesonide to reduce airway inflammation of asthmatic mice, but it is not obvious to improve ThlTh2 imbalance. Inhaled budesonide ① ability to reduce asthma host antibacterial reaction CRAMP expression of activation in the lung tissue; ② weaken asthma host bacterial clearance; ③ increased allergen-induced airway inflammation and bacterial infection. Inhaled corticosteroids inhibit asthma the host bacterial defense reaction.

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CLC: > Medicine, health > Internal Medicine > Respiratory system and chest diseases > Trachea and bronchial disease > Bronchial disease > Bronchial asthma
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