کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5859570 | 1562358 | 2012 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tumor necrosis factor-α mediates interactions between macrophages and epithelial cells underlying proinflammatory gene expression induced by particulate matter
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کلمات کلیدی
MIPregulated upon activation normal T cell expressed and secretedmTORCTNFRTNFUPMSRMMCPJnkmonokine induced by interferon-gammaLPSc-Jun N-terminal kinase - C-Jun N-terminal kinaseMIG - MEinterleukin - اینترلوکینanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancetumor necrosis factor-α - تومور نکروز عامل αUrban particulate matter - ذرات شهریparticulate matter - ذرات معلقCytokines - سیتوکین هاgranulocyte colony-stimulating factor - فاکتور تحریک کننده کلنی گرانولوسیتVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)G-CSF - فاکتور محرک کُلونی گرانولوسیتlipopolysaccharide - لیپوپلی ساکاریدstandard reference material - مرجع استانداردRANTES - مطالبMammalian target of rapamycin complex - هدف پستانداران مجتمع رپامایسینmacrophage inflammatory protein - پروتئین التهابی ماکروفاژmonocyte chemoattractant protein - پروتئین شیمیایی monocyte chemoattractantinterferon gamma-induced protein - پروتئین ناشی از گاما اینترفرون
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Ambient particulate matter (PM) exposure is known to have adverse effects on respiratory health, but the underlying mechanisms remain obscure. We tested the hypothesis that macrophages and epithelial cells synergize to produce maximal cytokine release in response to PM exposure, thereby promoting inflammatory responses. We developed a co-culture model using MLE-12 (mouse lung epithelial) cells and RAW 264.7 (mouse monocyte/macrophage) cells. MLE-12 cells produced KC (Cxcl1) but not tumor necrosis factor-α (TNF), and KC was upregulated only at high levels of urban particulate matter (UPM; NIST 1648a). RAW 264.7 cells produced TNF but not KC, and TNF production was increased by treatment with UPM. In contrast, KC production was upregulated by co-culture of MLE-12 and RAW 264.7 cells, and it was further increased by treatment with a concentration of UPM that had no effect on MLE-12 cells alone. Multiplex cytokine assay revealed a similar pattern of synergistic production of MIG (Cxcl9) and IP-10 (Cxcl10) in co-cultures in response to UPM. TNF was implicated as mediating the synergistic increase in KC production because TNF upregulated KC production in MLE-12 cells, and UPM-induced KC production in co-cultures could be inhibited by a TNF blocking antibody. Intratracheal instillation of UPM into both wild-type and TNF receptor knockout mice resulted in increased TNF production in lavage fluid and increased TNF mRNA expression in cells recovered from lavage fluid. Additionally, UPM instillation into wild-type mice resulted in increased neutrophils and KC in lavage fluid, and these were inhibited in UPM-exposed TNF receptor knockout mice. These results are consistent with a model in which PM activates TNF production in macrophages which in turn stimulates epithelial cells to produce proinflammatory cytokines such as KC. The findings suggest a potential mechanism by which inhaled PM induces inflammation in the lung.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 299, Issues 2â3, 28 September 2012, Pages 125-132
Journal: Toxicology - Volume 299, Issues 2â3, 28 September 2012, Pages 125-132
نویسندگان
Sadiatu Musah, Natasha DeJarnett, Gary W. Hoyle,