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

Jang Eun Cho, Yoon Suk Kim, Sangjung Park, Sang Nae Cho, Hyeyoung Lee

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Chemokines function in the migration of circulating leukocytes to regions of inflammation, and have been implicated in chronic inflammatory conditions including myco-bacterial 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.

Original languageEnglish
Pages (from-to)35-39
Number of pages5
JournalMolecules and cells
Volume29
Issue number1
DOIs
Publication statusPublished - 2010 Jan 1

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All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

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