| ObjectiveAir pollution is always an environmental problem concerned by all over the world. But domestic study on lung injury caused by air mixed pollutants has hardly none. With rapid development of industry and human living level, particular matter (PM) in air has been increasing especially PM10, whose diameter is less than 10 μxm. PM10 can enter directly respiratory tract because of its size. SO2 and NO2 liberated by burning of coal has also been increasing continuously. Air mixed pollutants of PM10, SO2 and NO2 can penetrate bronchi and alveoli with inhalation to cause respiratory diseases.To investigate the mechanism of lung injury caused by air mixed pollutants has been attentioned. Nowadays majority think lung injury caused by air pollutants is concerned with imbalance of inflammatory responses. T - auxiliary cell 1 ( Th - 1) can secrete pro - inflammatory cell factors such as interferon - γ (IFN - γ) and Th - 2 cell can secrete anti - inflammatory cell factors such as inter-leukin -4 (IL -4). So Th - 1/Th -2 imbalance may reflect the imbalance of inflammation and anti - inflammation. IFN - γ is a kind of glycoprotein secreted by Th - 1 cell. In immune responses IFN - y may induce cell differentiation from Th - 1 to Th -2 cell to inhibit synthesis of Th -2 cell factors. Thus IFN -y may regulate the development and prognosis of acute inflammation.Clara cell secretory 16 - kD protein (CC16) is one of the most dominant secretion of clara cell. CC16 may express mostly in lung and bronchi and its concentration in bronchoalveolar lavage fluid (BALF) has been thought to be high. Thus CC16 level in BALF may become a marker to measure the degree oflung injury.In this experiment we established animal model patterns with air mixed pollutants (PM10^SO2^NO2^CO) challenged, and quantitatively measured CC16 and IFN - 7 levels in BALF respectively to investigate the mechanism of lung injury.Method1. Preparation of air mixed pollutants(1) Collection of PM10 in pollutant areas —> preparation of PM10 mixture liquid with normal saline (N. S. ) .(2) Mixed gas of SO2,NO2 and CO is supplied by Dalian Specialized Gas Company.2. Establishment of animal model patternsWistar mice are divided into 4 groups------three experimental challengedgroups and one control group. With intratracheal instillation of PM10 mixture liquid and inhalation of air mixed gas of S02, N02 and CO in three experimental groups and with intratracheal instillation of normal saline and inhalation of normal air gas in one control group, we may establish the animal model patterns of lung injury caused by air mixed pollutants challenged. On the 1st, 7th and 30th day after inhalation of air mixed gas, we can get BALF with normal saline lava-ging bronchi and alveoli of Wistar mice.3. Utilization of ELISA to measure IFN - 7 level in BALF4. Utilization of western blotting to measure CC16 level in BALFResult1. IFN - 7 level in BALF: Compared with control group, IFN - 7 level in BALF increases in Id group and decreases in 7d and 30d groups.2. CC16 level in BALF: Compared with control group, CC16 level in BALF decreases dominantly in Id and7d groups and has significant meaning (pConclusion1. CC16 level in BALF is an important marker for acute lung injury caused by air mixed pollutants polluted.2. The mechanism of lung injury induced by air mixed pollutants polluted is probably due to imbalance of inflammatory responses. |