| Objective: Smoking is a major dangerous factor associated with humanbeing health, which can significantly increase the rate of respiratory tractinfections, coronary heart diseases and cancers. Epidemiological data showsalthough people’s smoking rate has shown a downward trend, the status ofpassive smoking did not. In our country, the number of death caused bysmoking-related diseases have been growing year by year. As the organinterlinked with the outside world, the lung will be the first to be affected,even the worst being affected. Whether the cigarette smoke is active or passiveinhaled into human body, it can cause respiratory tract mucosa injured andresult in chronic inflammation. Researches indicate that many cells andcytokine have been confirmed to participate in the pathogenesis of lung injurycaused by smoking. With the further research on T lymphocytes, it was foundthat the expression CD4+T cells (Thl7) increased in smoking-related lungdiseases, such as chronic obstructive pulmonary disease (COPD).Interleukin-17(IL-17) is the most representative cytokine produced by anewly identified T-cell subpopulation (Thl7). A large number of studies haveshown that IL-17is a pro-inflammatory cytokine, which can significantlystimulate the aggregation and excitation of neutrophil then cause the body toproduce powerful inflammatory response. Most of the research is focused onthe role of interleukin17in autoimmune diseases. However, the research onthe effect of interleukin17in smoking-related disease is less and themechanism remains unclear.We developed a lung injury rat model in which the animals were exposedto cigarette smoke. By well control of the time of passive smoking, we soughtto investigate the effects of both passive smoking and smoking cessation onlung tissue by examining histopathology assessment of lung. We also sought to investigate the effects of passive smoking and smoking cessation on thegrowth and development of rats by examining the general situation andweights of them. We discussed the mechanism of smoking-related lung injuryby examining the expression of IL-17in serum and lung tissue. In order tostrengthen human’s awareness of the smoking hazard to health and provide thetheoretical principle for quitting smoke movement.Methods: Fifty male Wistar rats of clean grade were randomly andequally divided into five groups: normal control group (NC),4-week passivesmoking group (4PS）,8-week passive smoking group (8PS)，12-week passivesmoking group (12PS) and smoking cessation group (CS). Passive smokinggroups were established by different length of time such as4or8or12weeksand normal control group in non-smoking environments. Narcotized with anintraperitoneal injection of Pentobarbital sodium3%, bloodletting fromAbdominal aorta and collected the serum, centrifuged it and drew out thesupernatant fluid and detected the contents of IL-17by ELASA. Sacrificed theanimals by open-chest, taken the inferior lobe of right lung, fixed by4%paraformaldehyde solution, conventional paraffin-embedded, sliced, HEstaining, observed the pathomorphism changes of lung tissue. The levels ofIL-17in lung tissue were detected by immunohistochemistry method.Results:1The fur of all rats of the passive smoking groups gradually becameyellow and fall off and the color brightness declined. The longer duration ofpassive smoking, the more significant of this phenomenon became, especiallyin the12-week passive smoking group. Some features of the smokingcessation group rats, such as action, fur color and brightness, are bettercompared with the12-week passive smoking group, but still not as good as thenormal control group.2The weight of rats in passive smoking groups were significantly slowerthan those in normal control group(P＜0.05). The weights of4PS were notstatistics different compared with NC group (P＜0.05).The weights of8PSgroup were significantly slower compared with NC group (P＜0.05) as well as between12PS group and NC group. There were no statistics difference in thecomparison of weight change between CS group and NC group.3HE staining: In normal control group, the structure of airway andalveolar are complete; The airway epithelium is damaged in passive smokinggroups. Such phenomenon of cilia lodging, irregular arrangement and somefall-off were observed. A large number of neutrophil infiltration were seenaround the airway wall. The longer duration of passive smoking, the moresignificant of the phenomenon，especially in passive smoking12-week group.In addition, the damage on rats’ lungs deepen and the alveolar wall expandedand became thinner, pulmonary emphysema were especially observed in12-week passive smoking group. Inflammatory cells infiltration andemphysema can still be observed in smoking cessation group, but the lesionwas reduced compare with12PS group.4The levels of IL-17in serum of rats in passive smoking groups weresignificantly higher than those in normal control group (P＜0.05). IL-17levelswere significantly different (P＜0.05) among4PS,8PS and12PS group. Thelevels of IL-17in serum in SC group were significantly higher comparedwith normal control group (P＜0.05), and lower compared with12PS group(P＜0.05), but there is no statistics difference between CS group and8PSgroup(P＞0.05).5The expression of IL-17in airway epithelium can be obviouslyobserved in all passive smoking groups. The expressions of IL-17in airwayepithelium gradually became deeper as the duration of passive smokingbecame longer: light yellow in4PS, claybank in8PS and tawny in12PS. Thecolor of airway epithelium of rats in smoking cessation group becameshallower but were as same as the8PS group.Conclusions:1Passive smoking could affect the growth of rats and slow down theirweight gain.2Passive smoking could cause a lot of inflammatory cell infiltration inthe rat’s lung tissue, further cause alveolar walls structure damaged, lead to pulmonary emphysema. Passive smoking for12weeks resulted in chronicbronchitis and emphysema.3The expression of IL-17significantly increased in serum and lungtissue of rats under passive smoking surrounding. The results suggested thatIL-17may be implicated in the pathogenesis of lung injury caused by passivesmoking.4Quitting smoking can relieve lung injury caused by passive smoking. |
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