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This Article Full Text Full Text (PDF) All Versions of this Article: 295/1/L220    most recent 90204.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Chmura, K. Articles by Chan, E. D. PubMed PubMed Citation Articles by Chmura, K. Articles by Chan, E. D.

Induction of IL-8 by Mycoplasma pneumoniae membrane in BEAS-2B cells

¹Department of Medicine, ²Program in Cell Biology, National Jewish Medical and Research Center, ³Denver Veterans Administration Medical Center; and ⁴Division of Pulmonary Sciences and Critical Care Medicine, ⁵University of Colorado School of Medicine, Denver, Colorado

Submitted 22 February 2008 ; accepted in final form 10 May 2008

Mycoplasma pne umoniae 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, and rarely bronchiectasis. In such disorders, neutrophil infiltration of the airways predominates. More recently, M. pneumoniae has been implicated in the pathogenesis of asthma. Epithelial cells play an important role in recruiting inflammatory cells into the airways. Since M. pneumoniae infection of human epithelial cells induces expression of IL-8—a potent activator of neutrophils—we investigated the signaling and transcriptional mechanisms by which mycoplasma membrane induces expression of this chemokine. In BEAS-2B human bronchial epithelial cells, mycoplasma membrane fraction (MMF) increased IL-8 mRNA and protein production. Activation of the transcriptional elements activating protein-1, nuclear factor-interleukin-6, and particularly NF-B are essential for optimal IL-8 production by MMF. The mitogen-activated protein kinases individually played a modest role in MMF-induced IL-8 production. Toll-like receptor-2 did not play a significant role in MMF-induction of IL-8. Antibiotics with microbicidal activity against M. pneumoniae are also known to have anti-inflammatory effects. Whereas clarithromycin, azithromycin, and moxifloxacin individually were able to inhibit TNF--induction of IL-8, each failed to inhibit MMF-induction of IL-8.

mollicutes; chemokines; gene regulation; toll-like receptors