Effects of diesel exhaust on murine alveolar macrophages and a macrophage cell line
Effects of diesel exhaust on murine alveolar macrophages and a macrophage cell line
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DOI：
10.1080/019021402753570509
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发表时间：
2002-04-01
影响因子：
1.7
通讯作者：
Sugawara, I
中科院分区：
文献类型：
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作者：
Saito, Y;Azuma, A;Sugawara, I
为了研究柴油机尾气颗粒物（DEP）和分枝杆菌注射对巨噬细胞的影响，我们检测了各种细胞因子（包括肿瘤坏死因子-α）的蛋白质和mRNA表达水平BALB/c小鼠肺泡巨噬细胞（AM）和巨噬细胞系中的TNF-α、白细胞介素（IL）-1 β、IL-12和IL-18（RAW 264.7）在体外用柴油机废气（DE）刺激后，用和不用牛分枝杆菌卡介苗（BCG）。将细胞暴露于体外系统中新鲜产生的DE。当AM暴露于DE（平均DEP暴露水平，300 mug/m3）时，TNF-α和IL-12的水平显著降低（TNF-α降低51%至61%，IL-12降低69%至78%），而IL-1 β和IL-18的水平保持不变。AM经DE处理后再经BCG处理，TNF-α水平较单独BCG处理的AM下降45%~ 71%，IL-1 β水平较单独BCG处理的AM上升154%。同样地，用含有抗M的DF刺激RAW264.7细胞。逆转录-聚合酶链反应（RTPCR）检测BCG和细胞因子mRNA水平。长期暴露于DE降低了RAW 264.7细胞中的TNT-α和IL-12 mRNA水平。当细胞暴露于DE并随后用BCG处理时，与单独用BCG处理的细胞相比，TNF-α、IL-1 β和IL-12 mRNA的水平降低。这些结果表明DE暴露对AM产生细胞因子具有复杂和多样的影响，并且较长的暴露（> 8小时）可以抑制AM在体外产生细胞因子。因此，长期暴露于DE可能会抑制肺部的宿主防御，并可能增加对肺部感染（如分枝杆菌感染）的易感性。
To investigate the effects of diesel exhaust particles (DEP) and mycobacterial injection on macrophages, we examined protein and mRNA expression levels of various cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-12, and IL-18 in BALB/c mouse alveolar macrophages (AM) and a macrophage cell line (RAW264.7) after in vitro stimulation with diesel exhaust (DE), with and without Mycobacterium bovis bacillus Calmette-Guerin (BCG). The cells were exposed to DE freshly generated in an in vitro system. When AM were exposed to DE (mean DEP exposure level, 300 mug/m(3)), the levels of TNF-alpha and IL-12 decreased significantly (by 51% to 61% for TNF-alpha and by 69% to 78% for IL-12), whereas those of IL-1beta and IL-18 remained unchanged. When AM were exposed to DE and then treated with BCG, the level of TNF-alpha decreased In 45% to 71%, whereas the level of IL-1beta increased by 154%, compared with AM treated with BCG alone. Similarly, RAW264.7 cells were stimulated with DF with anti without M. bovis BCG and cytokine mRNA levels examined by reverse transcriptase-polymerase chain reaction (RTPCR). Longer exposure to DE decreased TNT-alpha and IL-12 mRNA levels in the RAW264.7 cells. When the cells were exposed to DE and subsequently treated with BCG, levels of TNF-alpha, IL-1beta, and IL-12 mRNAs decreased compared with those of cells treated with BCG alone. These results show that DE exposure has complex and diverse effects on cytokine production by AM, and that longer exposure (> 8 hours) may suppress cytokine production by AM in vitro. Longer exposure of DE may therefore suppress the host defense in the lung and may increase susceptibility to lung infections such as mycobacterial infection.