Volume 137, Issue 2 pp. 341-350

Escherichia coli up-regulates proinflammatory cytokine expression in granulocyte/macrophage lineages of CD34+ stem cells via p50 homodimeric NF-κB

J. M. KIM

Corresponding Author

J. M. KIM

Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul,

Jung Mogg Kim MD, Department of Microbiology, Hanyang University College of Medicine, 17 Haengdang-dong, Sungdong-gu, Seoul 133–791, Korea.
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Y.-K. OH

Y.-K. OH

Department of Microbiology, Pochon CHA University College of Medicine, Kyunggi-do,

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Y.-J. KIM

Y.-J. KIM

Department of Science, Joongbu University, Choongnam,

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J. YOUN

J. YOUN

Department of Anatomy and Cell Biology, Hanyang University College of Medicine, Seoul, and

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M.-J. AHN

M.-J. AHN

Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea

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First published: 30 June 2004
Citations: 18

SUMMARY

Umbilical cord blood has emerged as an alternative source of haematopoietic CD34+ cells for allogeneic stem cell transplantation. Although bacteraemia induced by Escherichia coli is considered one of the complications of transplantation, expression of proinflammatory cytokines is poorly understood. In this study, we report the altered expression of proinflammatory cytokines in CD34+ cells and their in vitro cultured cells following E. coli infection. CD34+ stem cells and their cultured cells up-regulated expression of proinflammatory cytokines such as interleukin (IL)-1α, IL-6, IL-8 and tumour necrosis factor (TNF)-α after infection with E. coli. Expression of the proinflammatory cytokines was generated mainly by the granulocyte-macrophage lineages. E. coli infection activated the signals of p50/p50 nuclear factor-kappaB (NF-κB) homodimers and IκB kinase. Furthermore, inhibition of NF-κB activation lowered the up-regulated expression of the proinflammatory cytokines. These results suggest that CD34+ cells and their cultured cells infected with E. coli induce the expression of proinflammatory cytokines via the NF-κB pathway.

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