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http://dx.doi.org/10.5483/BMBRep.2013.46.4.200

Mycobacterium tuberculosis-induced expression of granulocyte-macrophage colony stimulating factor is mediated by PI3-K/MEK1/p38 MAPK signaling pathway  

Cho, Jang-Eun (Department of Biomedical Laboratory Science, Daegu Health College)
Park, Sangjung (College of Health Sciences, Yonsei University)
Lee, Hyeyoung (College of Health Sciences, Yonsei University)
Cho, Sang-Nae (Department of Microbiology, Yonsei University College of Medicine)
Kim, Yoon Suk (College of Health Sciences, Yonsei University)
Publication Information
BMB Reports / v.46, no.4, 2013 , pp. 213-218 More about this Journal
Abstract
Members of the colony stimulating factor cytokine family play important roles in macrophage activation and recruitment to inflammatory lesions. Among them, granulocyte-macrophage colony stimulating factor (GM-CSF) is known to be associated with immune response to mycobacterial infection. However, the mechanism through which Mycobacterium tuberculosis (MTB) affects the expression of GM-CSF is poorly understood. Using PMA-differentiated THP-1 cells, we found that MTB infection increased GM-CSF mRNA expression in a dose-dependent manner. Induction of GM-CSF mRNA expression peaked 6 h after infection, declining gradually thereafter and returning to its basal levels at 72 h. Secretion of GM-CSF protein was also elevated by MTB infection. The increase in mRNA expression and protein secretion of GM-CSF caused by MTB was inhibited in cells treated with inhibitors of p38 MAPK, mitogen-activated protein kinase kinase (MEK-1), and PI3-K. These results suggest that up-regulation of GM-CSF by MTB is mediated via the PI3-K/MEK1/p38 MAPK-associated signaling pathway.
Keywords
GM-CSF; MEK1; Mycobacterium tuberculosis; PI3-K; p38 MAPK;
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