Study On The Effect And Mechanism Of Ambient PM2.5 In The Pathogenesis Of Bronchial Asthma

Objective:The air fine particulate matter(PM2.5) is a liquid or solid matter dispersed in air,and its diameter is less than 2.5um. These particles are small enough to enter the alveolar to damage the human respiratory function, and then be absorbed into the pulmonary vascular endothelial cells, enter the blood circulation, and harm to the human body. It has been confirmed that there is a close correlation between air PM2.5standard and systemic diseases, such as cardiovascular and metabolic diseases. PM2.5is closely related to the risk of respiratory diseases, such as lung cancer, pulmonary tuberculosis, chronic obstructive pulmonary disease, asthma and so on. Bronchial asthma is a chronic reversible airflow limitation disease characterized by airway inflammation, airway hyperresponsiveness and airway remodeling. PM2.5 plays a role in the development of asthma. As a kind of pathogenic factor, can it cause the occurrence of bronchial asthma independently? Or works together with other pathogenic factors to increase the severity of asthma exacerbation? What is the pathogenesis of the disease? Is it to play a role in the effects of airway inflammation,airway hyperresponsiveness, and airway remodeling in a number of ways? The purpose of this study is to study and discuss the above issues, and to explain the role and mechanism of PM2.5 in the pathogenesis of bronchial asthma.Methods:Through the simulation of the human daily contact with air pollutants, to give the PM2.5 aerosol inhalation, OVA intraperitoneal injection sensitized, 1%OVA atomization inhalation challenged method to establish mouse animal model. Specific groups as follows: Control group, PM2.5 group, Asthma group, PM2.5+Asthma group, 6 mice per group, BALB/c mice(6–8 weeks of age). The effect of asthma in mice was evaluated from three aspects of airway heperresponsiveness, airway inflammation and airway remodeling.Results:1.Airway hyperresponsiveness: PM2.5 is not an independent pathogenic factor to increase airway hyperresponsiveness, nor as synergistic pathogenic factors in aggravating airway hyperresponsiveness of asthmatic mice.2. Airway inflammation:(1) counting the cell numbers in BALF: PM2.5 can not increase the numbers of eosinophils and lymphocytes alone in BALF, but can be as a synergistic pathogenic factors to increase eosinophil and lymphocyte count on the basis of asthmatic mice;(2) HE staining: PM2.5 can aggravate the inflammatory cells infiltration in the peribronchial and perivascular on the basis of asthmatic mice.It is suggested that the PM2.5 can not cause airway inflammation alone,but can be used as synergistic pathogenic factors to aggravate airway inflammation.3. Airway remodeling:(1) PAS staining: PM2.5 can cause airway mucus gland hyperplasia and increase mucus secretion on the basis of asthma;(2) Masson staining:PM2.5 can make the airway and vascular collagen fiber layer?smooth muscle layer thickene slightly on the basis of asthma;(3) ?-SMA immunohistochemistry: PM2.5can thicken the airway and vascular smooth muscle layer on the basis of asthma;(4)TGF-? immunohistochemistry: PM2.5 can increase the number of macrophage responsible for TGF-? production in the subepithelial peribronchiolar space slighely in normal mice,and make the macrophages where TGF-? stains brown increased significantly in asthmatic mice.So it is concluded that the PM2.5 cannot cause the occurrence of airway remodeling alone,but it can aggravate airway remodeling on the basis of asthma.4. Detection the expression of BALF TGF-? and plasma IgE:PM2.5 can increase the expression of BALF TGF-? on the basis of asthma, but it had no significant effect on the expression of plasma IgE.5.CBA cytokines Detection(IL-13, IL-17 A, 1L-1, GM-CSF,IL-1?): a differential expression of various cytokines in groups, the overall performance increased certain cytokines after treated with PM2.5 in the supernatant of mouse BALF expression.Conclusion:PM2.5 had no effect on airway hyperresponsiveness of bronchial asthma; PM2.5is not as independent risk factors in causing airway inflammation and airway remodeling, bu it can be as a synergistic pathogenic factors to aggravate airway inflammation and airway remodeling in asthmatic mice; PM2.5 can increase the secretion of certain cytokines.