The Influence Of Different Smoking Exposure Time On The Number Of Dendritic Cells

Objective: Smoking is one of the major factors influencing our health,which can lead to the diseases of Respiratory system, Diseases of thecardiovascular system and Tumor disease. According to the epidemiologicalsurvey data show,the number of people dying from smoking in china is around1million, which brings serious economic burden to the society. By studyingThe influence of different smoking exposure time on the number of dendriticcells (CD11c and S100), here this paper is trying to explore the dendritic cellschanges of lung tissue in early immune response caused by smoking in orderto provide immunology theory basis for early occurrence and developmentmechanism of respiratory system correlation diseases caused by smoking.Methods:50male Wistar rats (weight to150±20g),bought in animalsexperiment center of Hebei Medical University,animals qualified number(1309071),are raised in experimental Animal Room of People’s Hospital ofHebei province, and the animals rearing environment accords with clean gradeanimals feeding standard of Chinese experimental animals. Male Wistar ratswere randomly divided into5groups (10in each group): group A, blankcontrol; group B, smoking4weeks; group C, smoking8weeks; group D,smoking12weeks; group E, smoking8weeks and quit smoking8weeks. Byreference to a home-made experimental rat passive smoking device made byXu Sanlin etc, we made an organic glass case (70cm×60cm×40cm). Smokingexposure groups smoke twice a day (once in the morning and once in theafternoon, interval between each time is at least6hours or more),15cigaretteseach time, lasting about two hours. Intraperitoneal injection of3%sodiumpentobarbital anesthesia is given after smoking groups smoke4,8,12weeks,the middle lobe of the right lung is taken after abdominal aorta bleeds to death,fixed by4%paraformaldehyde, using paraffin embedding, then we observe pathology and measure the changes with immunohistochemical methodaccording to the expression of bronchial lung tissue CD11c and S100.Results:1changes of the general conditionAfter2weeks experiment, smoking exposure group rats start to burnout,lose hair luster, cough and increase respiratory tract secretion; At4th week,most of the rats show smoke irritation, and the concrete manifestation isrunning, impact in box, biting each other between the rats.2morphological changes of the lung tissuehematoxylin and eosin staining: lung tissue structure of blank controlgroup rats are normal.Obviousely, it can be seen from the Representativephotomicrographs of hematoxylin and eosin stained lung tissue, that alveolarstructure of blank control group rats are normal and uninjured.Bronchia don’thave inflammatory cell infiltration, alveolar walls are complete. Smokingexposure group and smoking cessation group both have different degree of ratbronchial ciliated epithelium breakage, falling off, around the walls show alarge number of mononuclear cells and lymphocyte infiltration, respiratorybronchioles present cystic.As for Group E(smoking8weeks and quit smoking8weeks), rats lung tissure and bronchial walls have inflammatory cellinfiltration, but compared to Group C, bronchial walls have less inflammatorycell infiltration.3comparison of the bronchial lung tissue CD11c proteinimmunohistochemical resultsCD11c+dendritic cells are distributed clearly on the bronchial walls,inflammatory area and blood vessels. Compared with Group A（the blankcontrol group）, which has CD11c protein (8.83±0.77) level, the CD11cprotein expression of the other4groups is obviously higher.GroupB(smoking4weeks group) has CD11c protein (12.22±0.22); Group C(smoking8weeksgroup) has CD11c protein (14.91±1.31); Goup D (smoking12weeks group)has CD11c protein (16.03±2.39); Group E(smoking8weeks and quit smoking8weeks group) has CD11c protein (14.03±2.39), expressions are significantly elevated, GroupE（smoking12weeks group）is the most obvious. Differencesare statistically significant (P<0.05). The CD11c protein expression ofGroup D （smoking12weeks group） is obviously higher than that of GroupB（smoking4weeks group）. Compared Group E （smoking8weeks and quitsmoking8weeks group） with blank control group, the difference hasstatistical significance (P<0.05).4comparison of the bronchial lung tissue S100proteinimmunohistochemical results.S100+dendritic cells are distributed clearly on the bronchial walls,inflammatory area and blood vessels. Compared with Group A（the blankcontrol group）, which has S100protein (8.38±0.84) level, the S100proteinexpression of the other4groups is obviously higher. GroupB(smoking4weeks group) has S100protein (10.32±1.08); Group C(smoking8weeks group)has S100protein (12.54±1.25); Goup D (smoking12weeks group) has S100protein (14.23±1.65); Group E(smoking8weeks and quit smoking8weeksgroup) has S100protein (13.01±2.09), expressions are significantly elevated,GroupE（smoking12weeks group） is the most obvious. Differences arestatistically significant (P<0.05). The S100protein expression of Group D（smoking12weeks group） is obviously higher than that of Group B（smoking4weeks group）. Compared Group E （smoking8weeks and quitsmoking8weeks group） with blank control group, the difference hasstatistical significance (P<0.05).Conclusion:1smoking exposure can cause rat lung tissue inflammations change, asthe extension of smoking exposure time, rats lung tissue inflammationsbecome more obvious, and emphysema changes gradually emerge.2smoking exposure can cause an increase in the number of dendriticcells of lung tissue of rats. With the duration of smoking exposure time, lungtissue dendritic cells of rats increase, and a large number of dendritic cells aregathered in the area of inflammation. We can see that distribution of dendritic cells around blood vessel of inflammation area, which implies that dendriticcells may come from the blood.3Smoking cessation can’t reverse the change of rats lung tissue chronicinflammation, but can slow down the process of inflammation change. Afterquitting smoke, the number of inflammation cells of lung tissue decreases, andthere is also some reduction in the number of dendritic cells.