목 적 : M. pneumoniae는 하기도 감염의 주된 원인이며, 기도질환 및 천식과 연관이 있다고 알려져 있다. 말초혈액에서의 호산구 증식이 M. pneumoniae 폐렴환자에게서 나타난다는 보고들은 있지만 M. pneumoniae가 호산구를 활성화시키는 기전에 대한 연구는 없는 상태이다. 본 연구에서는 MPL이 호산구를 활성화하여 염증매개 물질을 발현시키는지를 알아보고자 하였다. 방 법 : 호산구 세포주인 EoL-1을 MPL과 배양한 후 IL-8의 생산, superoxide 생성 및 호산구 표면의 CD69, ICAM-1, CD11b, CD49d의 발현을 측정하였다. 또한 MPL에 의한 EoL-1 세포에서의 MAPKs의 역할을 조사하였다. 결 과 : MPL은 EoL-1 세포에서 시간과 용량에 비례하여 IL-8을 생성하였으나 superoxide anion의 생성과 CD69, ICAM-1, CD11b, CD49d의 발현은 유도하지 않았다. ERK inhibitor, JNK inhibitor, p38 MAPK inhibitor는 MPL에 의해 유도되는 IL-8의 생성을 억제하였으나 NF-κB inhibitor는 IL-8 생성을 억제하지 않았다. 결 론 : MPL은 EoL-1 세포에서 IL-8의 생성을 유도하였으며, MAPKs의 활성화가 이에 관여하는 것으로 생각된다. 앞으로의 연구에서는 매개물질의 유전자 촉진부위(promoter)의 어떤 부위에서 어떤 전사인자를 활성화시켜 물질들을 생산하는 지에 대한 연구가 이루어져야 할 것이다.

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)-κB. 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.

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)-κB. 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.

Mycoplasma pneumoniae, EoL-1 cells, Interleukin-8, Mitogen-activated protein kinases