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Modulation of IL-8 Boosted by Mycoplasma pneumoniae lysate in Human Airway Epithelial Cells

Authors
 Kyung Eun Lee ; Kyung Won Kim ; Myung Hyun Sohn ; Kyu Earn Kim ; Jung Yeon Hong 
Citation
 Journal of Clinical Immunology, Vol.33(6) : 1117~1125, 2013 
Journal Title
 Journal of Clinical Immunology 
ISSN
 0271-9142 
Issue Date
2013
Abstract
Mycoplasma pneumoniae, a major cause of community-acquired pneumonia, has been recognized as a trigger for asthma inception and exacerbation. The epithelial cells on the respiratory tract parasitized by M. pneumoniae exhibit a number of cytopathic effects as a result of local inflammation and stimulated host immune response. We investigated the interactions of signaling molecules regulating the release of IL-8 by the direct stimulation of M. pneumoniae lysate (MPL) in human airway epithelial cells. In human airway epithelial cells, MPL-induced IL-8 proteins were decreased by monoclonal anti-TLR2 antibody in a dose-dependent fashion, and significantly blocked by siRNA TLR2. The pharmacologic inhibitors of ERK, U0126 and PD98059, effectively reduced IL-8 expression and the active forms of ERK signaling molecules, as detected by anti-phosphorylated p44/42 antibody. The region spanning from -132 to +41 in the IL-8 promoter demonstrated the highest luciferase activity against MPL and the mutations of NF-κB and NF-IL6 entirely diminished the activity. After investigating transfections of the NF-κB and NF-IL6 reporter vectors, NF-IL6 activation was significantly induced by MPL stimulation, which was considerably decreased by U0126 and monoclonal anti-TLR2 antibody. These results indicate that MPL-induced IL-8 increase is transcriptionally regulated by NF-IL6 more than by NF-κB. Additionally, the activation of NF-IL6 is influenced by TLR2 and ERK signaling pathways in airway epithelial cells.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/87223
DOI
10.1007/s10875-013-9909-y
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Pediatrics
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
Yonsei Authors
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Link
 http://link.springer.com/article/10.1007%2Fs10875-013-9909-y
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