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KMID : 0578320100290010035
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Molecules and Cells
2010 Volume.29 No. 1 p.35 ~ p.39
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Mycobacterium tuberculosis-Induced Expression of Leukotactin-1 Is Mediated by the PI3-K/PDK1/Akt Signaling Pathway
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Cho Jang-Eun
Kim Yoon-Suk
Park Sangjung
Cho Sang-Nae
Lee Hyeyoung
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Abstract
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Chemokines function in the migration of circulating leukocytes to regions of inflammation, and have been implicated in chronic inflammatory conditions including mycobacterial infection. We investigated whether Leukotactin-1 (Lkn-1), a novel member of the CC-chemokines, is involved in the immune response of macrophages against Mycobacterium tuberculosis (MTB). In PMA-differentiated THP-1 cells, MTB infection in-creased mRNA expression of Lkn-1 in a dose-dependent manner. Lkn-1 induction peaked 12 h after infection, then declined gradually and returned to its basal level at 72 h. Secretion of Lkn-1 was elevated by MTB infection. The increase in expression and secretion of Lkn-1 caused by MTB was reduced in cells treated with inhibitors of phos-phatidylinositol 3-kinase (PI3-K), 3-phosphoinositide-dependent kinase 1 (PDK1) and Akt. MTB-induced Akt phosphorylation was blocked by treatment with a PI3-K inhibitor or a PDK1 inhibitor, implying that PI3-K, PDK1, and Akt are associated with the signaling pathway that up-regulates Lkn-1 in response to MTB. These results suggest that Lkn-1 is novel member of the group of chemokines that is released by macrophages infected with MTB.
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KEYWORD
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3-phosphoinositide-dependent kinase 1, Akt, Leukotactin-1, Mycobacterium tuberculosis, phosphatidylinositol 3-kinase
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