Feedlot dust stimulation of interleukin-6 and -8 requires protein kinase Cepsilon in human bronchial epithelial cells.
Feedlot dust stimulation of interleukin-6 and -8 requires protein kinase Cepsilon in human bronchial epithelial cells.
复制标题
饲养场灰尘对白细胞介素 6 和 -8 的刺激需要人支气管上皮细胞中的蛋白激酶 Cepsilon。
DOI：
10.1152/ajplung.00103.2007
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发表时间：
2007
期刊：
影响因子：
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通讯作者：
Romberger,DebraJ
中科院分区：
文献类型：
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作者：
Wyatt,ToddA;Slager,RebeccaE;Devasure,Jane;Auvermann,BrentW;Mulhern,MichaelL;VonEssen,Susanna;Mathisen,Tracy;Floreani,AnthonyA;Romberger,DebraJ
Individuals exposed to dusts from concentrated animal feeding operations report increased numbers of respiratory tract symptoms, and bronchoalveolar lavage samples from such individuals demonstrate elevated lung inflammatory mediators, including interleukin (IL)-8 and IL-6. We previously found that exposure of bronchial epithelial cells to hog barn dusts resulted in a protein kinase C (PKC)-dependent increase in IL-6 and IL-8 release. We hypothesized that cattle feedlot dusts would also generate bronchial epithelial interleukin release in vitro. To test this, we used interleukin ELISAs and direct PKC isoform assays. We found that a dust extract from cattle feedlots [feedlot dust extract (FLDE)] augments PKC activity of human bronchial epithelial cells in vitro. A 5–10% dilution of FLDE stimulated a significant release of IL-6 and IL-8 at 6–24 h in a PKC-dependent manner vs. control medium-treated cells. An increase in PKCα activity was observed with 1 h of FLDE treatment, and PKCε activity was elevated at 6 h of FLDE exposure. The PKCα inhibitor, Gö-6976, did not inhibit FLDE-stimulated IL-8 and IL-6 release. However, the PKCε inhibitor, Ro 31-8220, effectively inhibited FLDE-stimulated IL-8 and IL-6 release. Inhibition of FLDE-stimulated IL-6 and IL-8 was confirmed in a dominant-negative PKCε-expressing BEAS-2B cell line but not observed in a PKCα dominant negative BEAS-2B cell line. These data support the hypothesis that FLDE exposure stimulates bronchial epithelial IL-8 and IL-6 release via a PKCε-dependent pathway.
