| Title |
Expression of c-Myc Is Related to Host Cell Death Following Salmonella typhimurium Infection in Macrophage |
| Author |
Jihyoun Seong1, Hong Hua Piao1, Phil Yeoul Ryu1, Youn Uck Kim2, Hyon E Choy1, and Yeongjin Hong1,3* |
| Address |
1Clinical Vaccine R&D Center, Chonnam National University Medical School, Gwangju 501-746, Republic of Korea, 2Department of Biomedical Sciences, Sun Moon University, A-San 336-708, Republic of Korea, 3Department of Microbiology, Chonnam National University Medical School, Gwangju 501-746, Republic of Korea |
| Bibliography |
Journal of Microbiology, 47(2),214-219, 2009,
|
| DOI |
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| Key Words |
Salmonella typhimurium, c-Myc, infection, ornithine decarboxylase, macrophage, cell death |
| Abstract |
It has been known that ornithine decarboxylase (ODC) induced by the binding of c-Myc to odc gene is closely linked to cell death. Here, we investigated the relationship between their expressions and cell death in macrophage cells following treatment with Salmonella typhimurium or lipopolysaccharide (LPS). ODC expression was increased by bacteria or LPS and repressed by inhibitors against mitogen-activated protein kinases (MAPKs) in Toll-like receptor 4 (TLR4) signaling pathway. In contrast, c-Myc protein level was increased after treatment with bacteria, but not by treatment with LPS or heat-killed bacteria although both bacteria and LPS increased the levels of c-myc mRNA to a similar extent. c-Myc protein level is dependent upon bacterial invasion because treatment with cytochalasin D (CCD), inhibitors of endocytosis, decreased c-Myc protein level. The cell death induced by bacteria was significantly decreased after treatment of CCD or c-Myc inhibitor, indicating that cell death by S. typhimurium infection is related to c-Myc, but not ODC. Consistent with this conclusion, treatment with bacteria mutated to host invasion did not increase c-Myc protein level and cell death rate. Taken together, it is suggested that induction of c-Myc by live bacterial infection is directly related to host cell death. |
