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CD14-dependent activation of NF-kappaB by filarial parasitic sheath proteins

Kishore Narayanan1, Bradly J Seufzer, Rebecca A Brockman-Schneider

  • 1Center for Biotechnology, Anna University, Chennai, 600 025, India.

Cell Biology International
|January 10, 2002
PubMed

Insights

Tropical pulmonary eosinophilia involves lung inflammation due to microfilariae. Filarial parasitic sheath proteins activate NF-kappaB, a key inflammation pathway, potentially involving CD14 on lung cells.

Area of Science:

  • Immunology
  • Cell Biology
  • Tropical Medicine

Background:

  • Tropical pulmonary eosinophilia (TPE) results from lung hyper-responsiveness to microfilariae.
  • Activation of transcription factor NF-kappaB is crucial for pro-inflammatory cytokine release in TPE.
  • The specific filarial antigens and cellular receptors involved in NF-kappaB activation remain unidentified.

Purpose of the Study:

  • To investigate the role of CD14 in NF-kappaB activation by filarial parasitic sheath proteins (FPS).
  • To determine if CD14 expression is sufficient for mediating FPS-induced NF-kappaB signaling.
  • To differentiate NF-kappaB activation pathways triggered by FPS from those induced by bacterial lipopolysaccharide (LPS).

Main Methods:

  • Utilized HEp-2 human airway epithelial cells and other cell types.
  • Examined the effect of filarial parasitic sheath proteins (FPS) on NF-kappaB activation.
  • Assessed the role of CD14 cell surface expression in NF-kappaB signaling.
  • Compared NF-kappaB activation by FPS with that induced by bacterial lipopolysaccharide (LPS).

Main Results:

  • FPS-induced NF-kappaB activation can be enhanced by CD14 cell surface expression.
  • CD14 expression alone is insufficient to confer responsiveness to FPS.
  • NF-kappaB activation by FPS differs from LPS-induced activation, despite CD14's involvement in both.
  • Lung epithelial cells' capacity to interact with microfilarial antigens and activate NF-kappaB via CD14 may contribute to TPE.

Conclusions:

  • CD14 plays a modulatory role in NF-kappaB activation by filarial antigens in lung epithelial cells.
  • The specific mechanism of FPS recognition and signal transduction requires further investigation.
  • These findings offer insights into the pathogenesis of tropical pulmonary eosinophilia and potential therapeutic targets.

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