Effects of Mycoplasma Pneumoniae on Activation of Human Eosinophilic Leukaemia EoL-1 Cells.
- Author:
Eun Soo KIM
1
;
Kyung Eun LEE
;
Hea Sun YANG
;
Kyung Won KIM
;
Joon Young PARK
;
Myung Hyun SOHN
;
Kyu Earn KIM
Author Information
1. Department of Pediatrics and Institute of Allergy, Yonsei University College of Medicine, Seoul, Korea. kekim@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Mycoplasma pneumoniae;
EoL-1 cells;
Interleukin-8;
Mitogen-activated protein kinases
- MeSH:
Asthma;
Cell Line;
Child;
Eosinophilia;
Eosinophils*;
Humans*;
Intercellular Adhesion Molecule-1;
Interleukin-8;
JNK Mitogen-Activated Protein Kinases;
Mitogen-Activated Protein Kinases;
Mycoplasma pneumoniae*;
Mycoplasma*;
p38 Mitogen-Activated Protein Kinases;
Phosphotransferases;
Pneumonia;
Pneumonia, Mycoplasma*;
Superoxides;
Young Adult
- From:Pediatric Allergy and Respiratory Disease
2007;17(1):8-16
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Mycoplasma pneumoniae is a common cause of lower respiratory disease, especially in children and young adults. Several studies have suggested that respiratory infection by M. pneumoniae is associated with reactive airway disease and asthma. Though eosinophilia in peripheral blood are revealed in patients with mycoplasmal pneumonia, what is not known is the functional capacity of M. pneumoniae to activate human eosinophils. We investigated whether M. pneumoniae lysate (MPL) can activate human eosinophils to release inflammatory mediators. METHODS: Human eosinophilic leukemic cell lines, EoL-1 cells were incubated with MPL. Activation of EoL-1 cells was monitored by IL-8 production, superoxide production and surface expression of CD69, ICAM-1, CD11b, and CD49d. In addition, we examined the effect of MPL and the role of mitogen-activated protein kinases (MAPKs) on IL-8 expression in EoL- 1 cells. RESULTS: MPL induced IL-8 release in a time- and dose- dependent manner. However MPL did not induce superoxide anion production and CD69, ICAM-1, CD11b, and CD49d surface expression in EoL-1 cells. Pretreatment with mitogen-activated protein/extracellular signal- regulated kinase (ERK) [MEK] inhibitor PD98059, c-Jun N-terminal kinase (JNK) inhibitor II SP600125, and selective p38 MAPK inhibitor SB202190 inhibited MPL-induced IL-8 production, but the MPL stimulation had no effect on the activities of nuclear factor (NF)-kappaB. CONCLUSION: These observations suggest that MPL causes activation of EoL-1 cells, and activation of MAPKs by MPL may be one of the mechanisms that result in an increase of the production of IL-8.
