USEFULNESS OF QUANTIFERON-TB AS A DIAGNOSTIC TOOL TO DETECT PLEURAL TUBERCULOSIS

MAPK/ERK通路 医学 激酶 p38丝裂原活化蛋白激酶 A549电池 呼吸上皮 免疫学 炎症 发病机制 白细胞介素8 内科学 细胞生物学 生物
作者
Myung Hyun Sohn,Dookyung Yang,Junghun Huh,Soo-Keol Lee,Choonhee Son,Min-Ki Lee,Yunsung Kim,Eun-Ha Song,Chulhun Chang
出处
期刊:Chest [Elsevier]
卷期号:128 (4): 396S-396S 被引量:16
标识
DOI:10.1378/chest.128.1.322
摘要

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.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 x 10(4) 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.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 micromol/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.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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