Korean Journal of Pediatrics 2006;49(9):977-982.
Published online September 15, 2006.
Mycoplasma pneumoniae-induced production of proasthmatic mediators in airway epithelium
Kyung Won Kim1, Byung Chul Lee2, Kyung Eun Lee1, Eun Soo Kim1, Tae Won Song1, Mi Yeoun Park2, Myung Hyun Sohn1, Kyu-Earn Kim1
1Department of Pediatrics and Institute of Allergy, Yonsei University College of Medicine
2Rickettsial and Zoonotic Diseases Division, Seoul, Korea Department of Microbiology*, National Insti
인체 기관지 상피세포에서 Mycoplasma pneumoniae 감염에 의한 천식 매개물질의 발현
김경원1, 이병철2, 이경은1, 김은수1, 송태원1, 박미연2, 손명현1, 김규언1
1연세대학교 의과대학 소아과학교실 및 알레르기 연구소
2국립보건원 세균부 리케치아과
Correspondence: 
Kyu-Earn Kim, Email: kekim@yumc.yonsei.ac.kr
Abstract
Purpose
: There has been an increasing amount of literature concerning the association between Mycoplasma pneumoniae and asthma pathogenesis. Interleukin(IL)-6 stimulates the differentiation of monocytes, and can promote Th2 differentiation and simultaneously inhibit Th1 polarization. IL-8 is a potent chemoattractant and, it has been suggested, has a role in asthma pathogenesis. Nitric oxide (NO) synthesized by airway epithelium may be important in the regulation of airway inflammation and reactivity. Vascular endothelial growth factor(VEGF) has been reported to be a mediator of airway remodeling in asthma. We investigated the effects of M. pneumoniae on IL-6, IL-8, NO and VEGF production in human respiratory epithelial cells.
Methods
: A549 cells were cultured and inoculated with M. pneumoniae at a dose of 20 cfu/cell. After infection, the presence of M. pneumoniae in epithelial cell cultures was monitored by immunofluorescence and confirmed by polymerase chain reaction(PCR) detection. IL-6, IL-8 and VEGF were determined by an enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction. NO was measured using the standard Griess reaction.
Results
: In A549 cells, M. pneumoniaeinduced IL-6, IL-8, NO and VEGF release in time-dependent manners. It also induced mRNA expression of IL-6, IL-8 and VEGF in similar manners.
Conclusion
: These observations suggest that M. pneumoniae might have a role in the pathogenesis of the allergic inflammation of bronchial asthma.


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