The Influence Of Endotoxin On The Expression Of ICAM-1, IL-6, IL-10 In The Lung Of Cigarette Smoke Exposed Rats

Background Currently, the numbers of smokers in China remains high and the number of deaths from smoking related diseases is rising year by year. In the harm of smoking to human body, bear the brunt of the respiratory system. The long-term chronic stimulation of cigarette smoke can lead to bronchi and pulmonary inflammation. In addition, the intrusion of endotoxin to lung can also induce lung inflammation.To the Long-term smokers, the infection can make the originally lung inflammation already existed even more serious and to develop chronic obstructive pulmonary disease, or acute respiratory distress syndrome, and multiple organ dysfunction.Objective To explore the influence of endotoxin on the expression of ICAM-1, IL-6, IL-10 in the lung of cigarette smoke exposed rats.Methods Forty healthy SD rats were randomly divided into 4 equal groups:LPS group,cigarette smoke group, the control group and the blank group, with ten rats in each group. The LPS group were exposed to cigarette smoke for 28 days, and was instilled with LPS through the trachea on the first day and the fourteenth day. The cigarette smoke group were only exposed to cigarette smoke for 28 days. The control group was instilled with physiological saline on the first day and the fourteenth day instead of LPS. The blank group is the non-treatment group. After 28 days,all rats were anaesthetized by 4% chloral hydrate solution (1mg·Kg-1), immobilized, implemented carotid artery catheterization, hen exposed diaphragm and linked with BL-420 biological signal collection and processing system. After 10 minutes, the breathing curve were recorded and the arterial blood were taken to test the arterial partial pressure of oxygen and the arterial partial pressure of carbondioxide, after the experiment, the lung tissue were also taken and divided into four parts, one was to observe the morphological changes of lung tissue by HE staining; one was to observe the expression of ICAM-1, IL-6 and IL-10 by immunohistochemical staining; one was to test the level of ICAM-1, IL-6 and IL-10 through ELISA; one was to detected the expression of ICAM-1, IL-6 and IL-10 mRNA by RT-PCR. All datas were retained and analysed through SPSS 13.0 statistical software.Results①According to the results of respiratory curve, compared with the cigarette smoke group, the inspiratory time, the expiratory time and the respiratory amplitude of the LPS group was shorted; compared with the blank group, the cigarette smoke group was shorted. Compared with the cigarette smoke group, the expiratory frequency of the LPS group was increased; compared with the blank group, the cigarette smoke group was increased. Compared with the control group, the cigarette smoke group have no statistical differences. ②According to the results of PaO2 and PaCO2, compared with the cigarette smoke group, the PaO2 of the LPS group was obviously lower, but the PaCO2 was obviously higher; compared with the blank group, the PaO2 of cigarette smoke group was obviously lower, but the PaCO2 was higher; compared with the control group, the PaO2 and the PaCO2 of the cigarette smoke group have no statistical differences. ③According to the results of the HE stainning, the LPS group have more serious inflammation pathological changes in the bronchial and alveolar; the cigarette smoke group and the control group also have the similar characteristics of the pathological changes, but to a lesser degree;the blank group have no above performance, and the bronchial and alveolar structure is normal.④ According to the results of immunohistochemical, compared with the cigarette smoke group, the expression of ICAM-1 and the IL-6 of the LPS group were higher, but the expression of IL-10 was lower; compared with the blank group, the expression of ICAM-1 and the IL-6 of the cigarette smoke group were higher, but the expression of IL-10 was lower; compared with the control group, the expression of ICAM-1, IL-6 and IL-10 of the cigarette smoke group have no statistical differences. ⑤According to the ELISA results, compared with the cigarette smoke group, the expression of ICAM-1 and the IL-6 of the LPS group were higher, but the expression of IL-10 was lower; compared with the blank group, the expression of ICAM-1 and the IL-6 of the cigarette smoke group were higher, but the expression of IL-10 was lower; compared with the control group, the expression of ICAM-1, IL-6 and IL-10 of the cigarette smoke group have no statistical differences. ⑥According to the results of RT-PCR, compared with the cigarette smoke group, the expression of ICAM-1, IL-6 mRNA of the LPS group were higher, but the expression of IL-10 mRNA was lower; compared with the blank group, the expression of ICAM-1, IL-6 mRNA of the cigarette smoke group were higher, but the expression of IL-10 mRNA was lower; compared with the control group, the expression of ICAM-1, IL-6, IL-10 mRNA of the cigarette smoke group have no statistical differences. All the results have statistical significance. (size of test a=0.05)Conclusion LPS can aggravate the lung inflammation and further reduce the respiratory function of the cigarette smoke treatment rats, The possible mechanism was related to the imbalance of inflammatory cascade reaction induced by the further increase of ICAM-1, IL-6 and the further induction of IL-10.