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c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in Mycobacterium tuberculosis-induced expression of Leukotactin-1

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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 p38MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1. [BMB Reports 2012;45(10): 583-588]

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 p38MAPK are involved in the signal pathway responsible for MTB-induced up-regulation of Lkn-1. [BMB Reports 2012;45(10): 583-588]

참고문헌 (32)

  1. WHO report 2007: Global tuberculosis control; surveillance, planning, financing, "World Health Organization", WHO, 277~ (2007)
  2. Law, K., "Increased release of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha by bronchoalveolar cells lavaged from involved sites in pulmonary tuberculosis", Am. J. Respir. Crit. Care. Med., 153, pp.799~804 (1996)
  3. Cooper, A. M., "The role of cytokines in the initiation, expansion, and control of cellular immuniy to tuberculosis", Immunol. Rev., 226, pp.191~204 (2008)
  4. Fenton, M. J., "Macrophages and tuberculosis", Curr. Opin. Hematol., 5, pp.72~78 (1998)
  5. Ferrara, G., "Mycobacterium tuberculosis induces CCL18 expression in human macrophages", Scand. J. Immunol., 68, pp.668~674 (2008)
  6. Peters, W., "Mechanisms of cell recruitment in the immune response to Mycobacterium tuberculosis", Microbes Infect., 5, pp.151~158 (2003)
  7. Hyun-Tak Jin, "Mechanism of T cell exhaustion in a chronic environment", BMB Reports, 44(4), pp.217~231 (2011), 생화학분자생물학회
  8. Majumder, N., "Restoration of impaired free radical generation and proinflammatory cytokines by MCP-1 in mycobacterial pathogenesis", Scand. J. Immunol., 67, pp.329~339 (2008)
  9. Lee, J. S., "Monocyte chemotactic protein-1 production in patients with active pulmonary tuberculosis and tuberculous pleurisy", Inflamm. Res., 52, pp.297~304 (2003)
  10. Algood, H. M., "Chemokines and tuberculosis", Cytokine Growth Factor Rev., 14, pp.467~477 (2003)
  11. Saukkonen, J. J., "Beta-chemokines are induced by Mycobacterium tuberculosis and inhibit its growth", Infect. Immun., 70, pp.1684~1693 (2002)
  12. Mendez-Samperio, P., "Mycobacterium bovis Bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways", Clin. Vaccine Immunol., 15, pp.277~283 (2008)
  13. Davis, J. M., "The role of the granuloma in expansion and dissemination of early tuberculous infection", Cell, 136, pp.37~49 (2009)
  14. Stegelmann, F., "Coordinate expression of CC chemokine ligand 5, granulysin, and perforin in CD8+ T cells provides a host defense mechanism against Mycobacterium tuberculosis", J. Immunol., 175, pp.7474~7483 (2005)
  15. Moser, B., "Chemokine; multiple levels of leukocyte migration control", Trends Immunol., 25, pp.75~84 (2004)
  16. Riedel, D. D., "Chemokine secretion by human polymorphonuclear granulocytes after stimulation with Mycobacterium tuberculosis and lipoarabinomannan", Infect. Immun., 65, pp.4620~4623 (1997)
  17. Karashima, K., "Elevated chemokine levels in bronchoalveolar lavage fluid of tuberculosis patients", Am. J. Respir. Crit. Care Med., 155, pp.1474~1477 (1997)
  18. Sadek, M. I., "Chemokines induced by infection of mononuclear phagocytes with mycobacteria and present in lung alveoli during active pulmonary tuberculosis", Am. J. Respir. Cell Mol. Biol., 19, pp.513~521 (1998)
  19. Zhang, Y., "Regulatory mechanisms of mitogen-activated kinase signaling", Cell Mol. Life Sci., 64, pp.2771~2789 (2007)
  20. Mendez-Samperio, P., "Mycobacterium bovis BCG induces CXC chemokine ligand 8 secretion via the MEK-dependent signal pathway in human epitheial cells", Cell Immunol., 234, pp.9~15 (2005)
  21. Roach, S. K., "Differential regulation of the mitogen-activated protein kinases by pathogenic and nonpathogenic mycobacteria", Infect. Immun., 70, pp.3040~3052 (2002)
  22. Méndez-Samperio, P., "Mycobacterium bovis Bacillus Calmette-Guérin (BCG) stimulates IL-10 production via the PI3K", Akt and p38 MAPK pathways in human lung epithelial cells, 2008, pp.251, 37~42
  23. A, S. K., "ESAT-6 induced COX-2 expression involves coordinated interplay between PI3K and MAPK signaling", Mol. Immunol., 49, pp.655~663 (2012)
  24. Sun Hwa Lee, "Transduced Tat-Annexin protein suppresses inflammationassociated gene expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells", BMB Reports, 44(7), pp.484~489 (2011), 생화학분자생물학회
  25. Obata, T., "MAP kinase pathways activated by stress: the p38 MAPK pathway", Crit. Care Med., 28, pp.67~77 (2000)
  26. Zhang, W., "MAPK signal pathways in the regulation of cell proliferation in mammalian cells", Cell Res., 12, pp.9~18 (2002)
  27. Surewicz, K., "The differential interaction of p38 MAP kinase and tumor necrosis factor-alpha in human alveolar macrophages and monocytes induced by Mycobacterium tuberculosis", Cell Immunol., 228, pp.34~41 (2004)
  28. Song, C. H., "Role of mitogen-activated protein kinase pathway in the production of tumor necrosis factor-alpha, interleukin-10, and monocyte chemotactic protein-1 by Mycobacterium tuberculosis H37Rv-infected human monocytes", J. Clin. Immunol., 23, pp.194~201 (2003)
  29. Lee, H. M., "Roles of Reactive Oxygen Species in CXCL8 and CCL2 Expression in Response to the 30-kDa Antigen of Mycobacterium tuberculosis", JOURNAL OF CLINICAL IMMUNOLOGY, 29, pp.46~56 (2009), SPRINGER[DOI]
  30. Youn, B. S., "Molecular cloning of leukotactin-1: a novel human beta-chemokine, a chemoattractant for neutrophils, monocytes, and lymphocytes, and a potent agonist at CC chemokine receptors 1 and 3", J. Immunol., 159, pp.5201~5205 (1997)
  31. Jang-Eun Cho, "Mycobacterium tuberculosis-Induced Expression of Leukotactin-1 Is Mediated by the PI3-K", PDK1, Molecules and Cells, pp.2010, 29(1)[DOI]
  32. Jae-Han Jeong, "Anti-inflammatory effects of ethanol extract from Orostachys japonicus on modulation of signal pathways in LPS-stimulated RAW 264.7 cells", BMB Reports, 44(6), pp.399~404 (2011), 생화학분자생물학회

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