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Mycobacterium tuberculosis-induced expression of Leukotactin-1 is mediated by the PI3-K/PDK1/Akt signaling pathway

Authors
 Jang-Eun Cho  ;  Yoon Suk Kim  ;  Sangjung Park  ;  Sang-Nae Cho  ;  Hyeyoung Lee 
Citation
 MOLECULES AND CELLS, Vol.29(1) : 35-39, 2010 
Journal Title
 MOLECULES AND CELLS 
ISSN
 1016-8478 
Issue Date
2010
MeSH
Cell Line, Tumor ; Chemokines, CC/genetics ; Chemokines, CC/immunology ; Chemokines, CC/metabolism* ; Chemotaxis ; Humans ; Macrophage Inflammatory Proteins/genetics ; Macrophage Inflammatory Proteins/immunology ; Macrophage Inflammatory Proteins/metabolism* ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism* ; Macrophages/microbiology ; Macrophages/pathology ; Mycobacterium tuberculosis/immunology* ; Mycobacterium tuberculosis/pathogenicity ; Oncogene Protein v-akt/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction/drug effects ; Signal Transduction/immunology* ; Tuberculosis/genetics ; Tuberculosis/immunology* ; Tuberculosis/metabolism
Keywords
3-phosphoinositide-dependent kinase 1 ; Akt ; Leukotactin-1 ; Mycobacterium tuberculosis ; phosphatidylinositol 3-kinase
Abstract
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 increased 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 phosphatidylinositol 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.
Full Text
http://link.springer.com/article/10.1007%2Fs10059-010-0003-5
DOI
10.1007/s10059-010-0003-5
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Institute for Immunology and Immunological Disease (면역질환연구소) > 1. Journal Papers
Yonsei Authors
Cho, Sang Nae(조상래)
Cho, Jang Eun(조장은)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/101945
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