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The acute pulmonary toxicity in mice induced by Staphylococcusaureus particulate matter and their combination

机译:金黄色葡萄球菌诱发的小鼠急性肺毒性金黄色颗粒物质及其组合

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摘要

Inhalation of pathogenic bacteria transported by particulate matter (PM) presents an important potential threat to human health. Therefore, the pulmonary toxicity in mice caused by Staphylococcus aureus (S. aureus) and PM as individual matter and mixtures was studied. PM and S. aureus were instilled intratracheally into Kunming mice at doses of 0.2 mg/mouse and 5.08 × 106 CFU /mouse, respectively, as individual matter and in combination two times at 5-day intervals. After the exposure period, oxidative stress markers and nitric oxide (NO) in the lung, cellular infiltration, neurotrophins, chemokines, and cytokines in bronchoalveolar lavage fluid (BALF), and immunoglobulin (Ig) in sera were examined. Exposure to the combination of PM and S. aureus caused significant increases in malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and NO and significant decreases in total antioxidant capacity (T-AOC) and the ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG) in the lung. Meanwhile, the ratio of interleukin (IL)-4 to interferon (INF)-γ, the IL-4 level in BALF, and the IgE concentration in sera were significantly increased in the groups exposed to S. aureus or the combination of PM and S. aureus. Substance P and IL-8 in BALF weresignificantly increased in mice exposed to PM, S. aureus or theircombination. In addition, PM, S. aureus, and their combination causedinfiltration of leukocytes into the alveolar tissue spaces. The results suggested thatexposure to the combination of PM and S. aureus induced a lunginflammatory response that was at least partly caused by oxidative stress and mediatorsfrom the activated eosinophils, neutrophils, alveolar macrophages, and epithelialcells.
机译:吸入由颗粒物(PM)输送的致病细菌对人体健康构成了重要的潜在威胁。因此,研究了由金黄色葡萄球菌(S. aureus)和PM作为单独物质和混合物引起的小鼠肺部毒性。将PM和金黄色葡萄球菌分别以0.2 mg /小鼠和5.08×10 6 CFU /小鼠的剂量分别气管内滴入昆明小鼠,每5天间隔两次。暴露期后,检查肺中的氧化应激标记物和一氧化氮(NO),支气管肺泡灌洗液(BALF)中的细胞浸润,神经营养蛋白,趋化因子和细胞因子,以及血清中的免疫球蛋白(Ig)。暴露于PM和金黄色葡萄球菌的组合会导致丙二醛(MDA),过氧化氢酶(CAT),超氧化物歧化酶(SOD)和NO的显着增加,总抗氧化能力(T-AOC)和还原型谷胱甘肽的比率显着降低(GSH)转化为肺中的氧化型谷胱甘肽(GSSG)。同时,暴露于金黄色葡萄球菌或PM和PM联合使用的组中,白介素(IL)-4与干扰素(INF)-γ的比率,BALF中的IL-4水平以及血清中的IgE浓度均显着增加。金黄色葡萄球菌。 BALF中的P和IL-8物质分别为在暴露于PM,金黄色葡萄球菌或其小鼠的小鼠中显着增加组合。另外,PM,金黄色葡萄球菌及其组合引起白细胞浸入肺泡组织间隙。结果表明暴露于PM和金黄色葡萄球菌的组合诱导肺炎症反应至少部分是由氧化应激和介体引起的来自活化的嗜酸性粒细胞,嗜中性粒细胞,肺泡巨噬细胞和上皮细胞细胞。

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