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Laboratory and Animal Investigations |

Effect of Mycoplasma pneumoniae Lysate on Interleukin-8 Gene Expression in Human Respiratory Epithelial Cells*

Myung Hyun Sohn, MD; Kyung Eun Lee, MSc; Sung Yon Choi, MD; Byoung Chul Kwon, MD; Myung Woong Chang, PhD; Kyu-Earn Kim, MD
Author and Funding Information

*From the Department of Pediatrics and Institute of Allergy (Drs. Sohn, Choi, Kwon, Kim, and Mr. Lee), BK21 Project for Medical Science, Yonsei University College of Medicine, Seoul; and Department of Microbiology (Dr. Chang), College of Medicine, Koshin University, Busan, Korea.

Correspondence to: Kyu-Earn Kim, MD, PhD, Department of Pediatrics, Yonsei University College of Medicine, Youngdong Severance Hospital, PO Box 1217, Seoul 135–270, Korea; e-mail: kekim@yumc.yonsei.ac.kr



Chest. 2005;128(1):322-326. doi:10.1378/chest.128.1.322
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Study objectives: Mycoplasma pneumoniae is a common cause of lower respiratory disease. Several studies have suggested that respiratory infection by M pneumoniae is associated with reactive airway disease and asthma. Interleukin (IL)-8 has been suggested to have a role in the pathogenesis of the allergic inflammation of bronchial asthma, and is well known to be expressed in bronchial epithelial cells.

Measurements: An examination was carried out into the effect of M pneumoniae lysate (MPL) and the role of mitogen-activated protein kinases (MAPKs) and extracellular signal-regulated kinase (ERK) on IL-8 expression in human lung epithelial cells. A549 cells were seeded at a density of 5 × 104 cells per well and incubated in basal medium for a further 24 h. IL-8 levels were determined by an enzyme-linked immunosorbent assay. MAPK phosphorylation was assessed by Western blotting.

Results: In A549 cells, MPL induced IL-8 release in a time- and dose-dependent manner. Pretreatment with PD 98059, which blocks the activation of MAPK/ERK kinase 1, inhibited MPL-induced IL-8 production by 64.4% at 25 μmol/L. Stimulation of A549 cells by MPL also caused an increase in the activity of ERK, compared with the nonstimulated cells. The MPL stimulation had no effect on the activities of p38.

Conclusion: These observations suggest that activation of ERK by MPL may be one of the mechanisms that result in an increase of the production of IL-8.

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