Effect of Mycoplasma pneumoniae lysate on interleukin-8 gene expression in human respiratory epithelial cells.
نویسندگان
چکیده
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 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. 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 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. 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.
منابع مشابه
Induction of IL-8 by Mycoplasma pneumoniae membrane in BEAS-2B cells.
Mycoplasma pneumoniae is an extracellular pathogen, residing on mucosal surfaces of the respiratory and genital tracts. The lack of cell walls in mycoplasmas facilitates the direct contact of the bacterial membrane with the host cell. The cell membrane of mycoplasma is the major inducer of the host pathogenic response. Airway diseases caused by M. pneumoniae include bronchiolitis, bronchitis, a...
متن کاملInduction of proinflammatory cytokines in human lung epithelial cells during Chlamydia pneumoniae infection.
Chlamydia pneumoniae is an obligate intracellular human pathogen that causes acute respiratory diseases such as pneumonia and bronchitis. Previous studies have established that C. pneumoniae can induce cytokines in mouse and/or human cells, but little information is available on the cytokine response of respiratory epithelial cells, a first line of infection. In this study, heparin treatment of...
متن کاملMycoplasma pneumoniae antigens stimulate interleukin-8.
A sthma is characterized by the presence of airway inflammation that results in bronchial hyperresponsiveness and symptoms of airway obstruction. Persistent and severe asthma may have an eosinophilic or noneosinophilic infiltration of the airways, the latter characterized by a profusion of neutrophils.1 More recent findings implicate that neutrophils may play a role in the irreversible airflow ...
متن کاملMycoplasma pneumoniae induces airway epithelial cell expression of MUC5AC in asthma.
As excess mucin expression can contribute to the exacerbation of asthma, the present authors hypothesised that Mycoplasma pneumoniae significantly induces MUC5AC (the major airway mucin) expression in airway epithelial cells isolated directly from asthmatic subjects. A total of 11 subjects with asthma and six normal controls underwent bronchoscopy with airway brushing. Epithelial cells were cul...
متن کاملTLR2 signaling is critical for Mycoplasma pneumoniae-induced airway mucin expression.
Excessive airway mucin production contributes to airway obstruction in lung diseases such as asthma and chronic obstructive pulmonary disease. Respiratory infections, such as atypical bacterium Mycoplasma pneumoniae (Mp), have been proposed to worsen asthma and chronic obstructive pulmonary disease in part through increasing mucin. However, the molecular mechanisms involved in infection-induced...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Chest
دوره 128 1 شماره
صفحات -
تاریخ انتشار 2005