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Induction of IL-8 by Mycoplasma pneumoniae membrane in BEAS-2B cells
Kathryn Chmura1, Xiyuan Bai, Mari Nakamura
1Department of Medicin, National Jewish Medical and Research Center, Denver, Colorado 80206, USA.
Abstract:
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, 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-kappaB 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-alpha-induction of IL-8, each failed to inhibit MMF-induction of IL-8.
Insights
Mycoplasma pneumoniae membrane triggers airway inflammation by inducing IL-8. This response is mediated by specific transcription factors, but not TLR-2, and is not inhibited by common antibiotics.
Area of Science:
- Immunology
- Microbiology
- Respiratory Medicine
Background:
- Mycoplasma pneumoniae is an extracellular pathogen that colonizes mucosal surfaces.
- Its cell membrane is a key factor in initiating host pathogenic responses, contributing to airway diseases like asthma.
- Epithelial cells are crucial in recruiting inflammatory cells, particularly neutrophils, to the airways.
Purpose of the Study:
- To investigate the signaling and transcriptional mechanisms by which the mycoplasma membrane induces Interleukin-8 (IL-8) expression in human bronchial epithelial cells.
- To identify the key transcription factors and signaling pathways involved in M. pneumoniae-induced IL-8 production.
- To assess the role of Toll-like receptor-2 (TLR-2) and the anti-inflammatory effects of antibiotics on this pathway.
Main Methods:
- Exposure of BEAS-2B human bronchial epithelial cells to mycoplasma membrane fraction (MMF).
- Measurement of IL-8 mRNA and protein production.
- Analysis of the involvement of transcription factors (AP-1, NF-IL-6, NF-kappaB) and mitogen-activated protein kinases (MAPKs).
- Assessment of TLR-2 involvement and the effect of antibiotics (clarithromycin, azithromycin, moxifloxacin) on MMF-induced IL-8.
Main Results:
- MMF significantly increased IL-8 mRNA and protein production in BEAS-2B cells.
- Activation of AP-1, NF-IL-6, and particularly NF-kappaB transcription factors was essential for MMF-induced IL-8 production.
- MAPKs played a modest role, and TLR-2 was not significantly involved in MMF-induced IL-8.
- While antibiotics inhibited TNF-alpha-induced IL-8, they failed to inhibit MMF-induced IL-8.
Conclusions:
- The mycoplasma membrane is a potent inducer of IL-8 in bronchial epithelial cells, primarily through NF-kappaB activation.
- This pathway is distinct from TLR-2 mediated responses and is not targeted by common macrolide antibiotics.
- Understanding these mechanisms is crucial for developing targeted therapies for M. pneumoniae-associated airway inflammation and asthma.
