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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  ;  Jung Yeon Hong  ;  Kyu Earn Kim  ;  Myung Hyun Sohn 
Citation
 JOURNAL OF CLINICAL IMMUNOLOGY, Vol.33(6) : 1117-1125, 2013 
Journal Title
JOURNAL OF CLINICAL IMMUNOLOGY
ISSN
 0271-9142 
Issue Date
2013
MeSH
Antibodies, Blocking/pharmacology ; Antigens, Bacterial/immunology ; Butadienes/pharmacology ; CCAAT-Enhancer-Binding Protein-beta/genetics ; CCAAT-Enhancer-Binding Protein-beta/metabolism ; Cells, Cultured ; Flavonoids/pharmacology ; Gene Expression Regulation* ; Genetic Engineering ; Humans ; Interleukin-8/genetics* ; MAP Kinase Signaling System ; Mycoplasma pneumoniae/immunology* ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Nitriles/pharmacology ; Promoter Regions, Genetic/genetics ; RNA, Small Interfering/genetics ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/immunology* ; Toll-Like Receptor 2/genetics ; Toll-Like Receptor 2/immunology ; Toll-Like Receptor 2/metabolism* ; Transcriptional Activation/drug effects ; Transcriptional Activation/genetics
Keywords
Mycoplasma pneumoniae ; airway epithelial cell ; IL-8 ; TLR2 ; ERK ; NF-IL6
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.
Full Text
http://link.springer.com/article/10.1007%2Fs10875-013-9909-y
DOI
10.1007/s10875-013-9909-y
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Kyung Won(김경원) ORCID logo https://orcid.org/0000-0003-4529-6135
Kim, Kyu Earn(김규언)
Sohn, Myung Hyun(손명현) ORCID logo https://orcid.org/0000-0002-2478-487X
Lee, Kyung Eun(이경은)
Hong, Jung Yeon(홍정연) ORCID logo https://orcid.org/0000-0003-0406-9956
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/87223
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