| The direct target organ of air pollution is the respiratory system, it is one of important factors to harm respiratory system. Some chronic respiratory system illnesses are related to air pollution closely. Exposure to air pollutants for a long time can cause human body immunity to be low, it also causes tracheitis, bronchial asthma and so on chronic sickness. At present the inflammatory damage mechanism of air pollution to organism respiratory system is not yet explicit. Through simulating air pollution present situation, determines the levels of TNF-α, IL-1, IL-6, IL-8, IL-4, IL-10, and IL-13 in BALF of rats to further discusses the inflammatory damage mechanism of air pollutant to the respiratory system of rats.Material and method 96 Wistar rats (provided by experimental animal center of China Medical University, weight 200~240g, half female and half male), are randomly divided into 9 experimental groups stochastically (lower 1d group, lower 15d group, lower 30d group, middle 1d group, middle 15d group, middle 30d group, high 1d group, high 15d group, high 30d group) and 3 control groups (control 1d group, control 15d group, control 30d group), each group 8 rats. Rats were intratracheally injected with 7.5, 15, 22.5mg PM10 suspended in 1ml saline for lower, middle, high dose groups respectively. And 1ml normal saline was intratracheally injected in rats of control group. The rats in lower, middle and high dose group were statically inhaled 12 times diluted SO2, NO2, CO mixed air. The concentrations of SO2, NO2, CO for lower dose groups were 7.5, 6, 200mg/m3, for middle dose group 15, 12, 400mg/m3, for high dose group 22.5, 18, 600 mg/m3 respectively. The exposure lasted for 30 days, 2 hours daily. Control group inhaled normal air. After inhaling air pollutant 1d, 15d, 30d, the rats were killed at the next day. Bronchoalveolar lavage was done with 37℃normal saline through trachea cannula, each time 3ml, washes 3 times, merge bronchoalveolar bavage fluids and centrifuge, put the supernate in the low temperature refrigerator of - 80℃preservation.The levels of IL-1, IL-6, IL-8, TNF-α, IL-4, IL-10, and IL-13 in BALF were determined by ELISA. The statistics analysis was carryed by SPSS10.0 software. The best curve regression equation were fitted, extracts various cytokines density in the sample; Uses single factor variance analysis in TNF-α, IL-1, IL-6, IL-8, IL-4, IL-10 and the IL-13 group level's comparison.ResultsThe pro-inflammatory cytokine levels of TNF-α, IL-1, IL-6 and the IL-8 in BALF of 1d group were obviously higher than that in control group; 15d group and 30d group level drops, there was significant statistics difference between 30d group and 1d group, the IL-6 expression level is the highest in pro-inflammatory cytokine, next for TNF-αand IL-8, the IL-1expression level is the lowest.The anti-inflammatory cytokine levels of IL-4, IL-10 and the IL-13 in BALF of 1d group were obviously higher than that of control group; 15d and the 30d group level drops, there was significant statistics difference between 30d group and 1d group, the IL-10 expression level is higher than IL-4 and IL-13.There was no significant statistics difference in inflammatory cytokines expression level among different dose groups.DiscussionThe cytokines (CKs) are small molecular multi-peptides synthesis and the secreted by the immune cell or the non-immune cell. It can adjust cell's growth, differentiation, organism immune function. It participate inflammation occurrence and wound cicatrization and so on. IL-6 is one of main acute inflammation response features, it participate organism inflammation response and anti-infection defense. The high TNF-αexpression level indicated that TNF-αmay promote IL-6 and the IL-8 production, IL-1 promote marrow release neutrophil, induce monocaryotic cell and the polynuclear granular cell infiltrate to the inflammation part, release lysosome enzyme to lead the partial inflammatory response, cause basophilic granulocyte and mast cell escape the granule, release inflammatory mediator, thus further intensifies the organism inflammatory reaction.In lung's acute inflammation time IL-10 suppresses IL-1, IL-6, IL-8 and TNF-αexpresses, but does not affect anti- inflammation medium such as IL-1 acceptor antagonist expression function, it advantageous is balanced in the reconstruction inflammation medium/ anti-inflammatory medium; IL-10 has obvious resistance inflammatory cells and so on lymphocyte and neutral granular cell the function which infiltrates in the lung organization, thus reduces the lung damage.Through suppressing the endothelial cell and single nuclear cell synthesis and secrete IL-l, IL-6 and TNF-α, IL-4 reduce endothelial cell's damage of inflammatory medium. Through strengthen Th2 activity to causes this kind of cell massively syntheses and secrete IL-4 and IL-10, finally form a reflection cycle synthesis by anti- inflammation cytokines, resist the organism excessive inflammatory response, IL-4 play the triggering reagent role during this process.IL-l3 may adjust the body inflammatory response through suppress production of hasten factor and inflammatory cytokines in the organization to played certain protective function.ConclusionsThrough simulating present air pollution situation, testing TNF-α, IL-1, IL-6, IL-8, IL-4, IL-10 and the IL-13 expression level in BALF demonstrating that inflammatory cytokines expression level exist time effect relations, but have no dose effect relations, it showed that the air pollutant may induce rats lung organization to release IL-6, IL-8, TNF-α, IL-1, IL-4, IL-10 and IL-13. IL-6 and TNF-αexpression level is higher in the pro-inflammatory cytokine. The anti-inflammatory cytokine IL-10 expression level is higher than IL-4 and IL-13, the anti-inflammatory cytokine expression level is lower than that of pro-inflammatory cytokine, thus cause lung organization inflammatory damage. Therefore, IL-6, TNF-α, and IL-10 may be as sensitive indexes for lung inflammation in early time result from air pollution.This text lay the foundation to the respiratory system damage mechanism research caused by air pollution through determining inflammatory cytokines level change in BALF. |
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