C-Jun n-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in mycobacterium tuberculosis-induced expression of leukotactin-1

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

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Leukotactin(Lkn)-1 is a CC chemokine and is upregulated in macrophages in response to Mycobacterium tuberculosis (MTB) infection. We investigated whether mitogen-activated protein kinases (MAPKs) are involved in MTB-induced expression of Lkn-1. The up-regulation of Lkn-1 by infection with MTB was inhibited in cells treated with inhibitors specific for JNK (SP600125) or p38 MAPK (SB202190). Since the up-regulation of Lkn-1 by MTB has been reported to be mediated by the PI3-K/PDK1/Akt signaling, we examined whether JNK and/or p38 MAPK are also involved in this signal pathway. MTB-induced Akt phosphorylation was blocked by treatment with JNK- or p38 MAPK-specific inhibitors implying that p38 and JNK are upstream of Akt. In addition, treatment with the PI3-K-specific inhibitor inhibited MTB-stimulated activation of JNK or p38 MAPK implying that PI3-K is upstream of JNK and p38 MAPK. These results collectively suggest that JNK and p38 MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1.

Original languageEnglish
Pages (from-to)583-588
Number of pages6
JournalBMB reports
Volume45
Issue number10
DOIs
Publication statusPublished - 2012

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Fingerprint Dive into the research topics of 'C-Jun n-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in mycobacterium tuberculosis-induced expression of leukotactin-1'. Together they form a unique fingerprint.

  • Cite this