• infectious immunity;
  • parasites;
  • lung;
  • transcription factors;
  • filariasis

Tropical pulmonary eosinophilia is in part caused by the hyperimmune responsiveness of the lung tissue against the antigens of degenerating microfilariae. We have previously shown that the activation of the transcription factor NF-κB is essential for the synthesis and release of multiple pro-inflammatory cytokines in HEp-2 human airway epithelial cells following exposure to filarial parasitic sheath proteins (FPS). Neither the antigenic component nor the receptor involved in this activation is known. Herein we provide evidence that FPS activation of NF-κB can be augmented by the cell surface expression of CD14. CD14 expression, however, is not sufficient to transduce FPS signals for NF-κB activation, since its expression in different cell types does not always furnish the capacity to respond to FPS. We also show that NF-κB activation by FPS treatment can be distinguished from that induced by bacterial lipolysaccharide, an agent that can also activate NF-κB in a CD14-dependent fashion. These observations suggest that the capacity of certain lung epithelial cells to interact with microfilarial antigens, activate NF-κB in a CD14-dependent manner and produce pro-inflammatory cytokines may be a contributory factor to immune responses manifested by tropical pulmonary eosinophilia.