title: CD14-dependent activation of NF-kappaB by filarial parasitic sheath proteins.
abstract: 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-kappaB 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-kappaB can be augmented by the cell surface expression of CD14. CD14 expression, however, is not sufficient to transduce FPS signals for NF-kappaB activation, since its expression in different cell types does not always furnish the capacity to respond to FPS. We also show that NF-kappaB activation by FPS treatment can be distinguished from that induced by bacterial lipolysaccharide, an agent that can also activate NF-kappaB in a CD14-dependent fashion. These observations suggest that the capacity of certain lung epithelial cells to interact with microfilarial antigens, activate NF-kappaB in a CD14-dependent manner and produce pro-inflammatory cytokines may be a contributory factor to immune responses manifested by tropical pulmonary eosinophilia.
authors.affiliation: Center for Biotechnology, Anna University, Chennai, 600 025, India.
authors.forename: Kishore
authors.initials: K
authors.lastname: Narayanan
authors.forename: Bradly J
authors.initials: BJ
authors.lastname: Seufzer
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Brockman-Schneider
authors.forename: James E
authors.initials: JE
authors.lastname: Gern
authors.forename: Arun
authors.initials: A
authors.lastname: Balakrishnan
authors.forename: Shigeki
authors.initials: S
authors.lastname: Miyamoto
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D015153:Blotting, Western; D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology; D004804:Eosinophils; D004847:Epithelial Cells / Q000378:metabolism / Q000382:microbiology; D006801:Humans; D020672:I-kappa B Proteins; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis*; D008168:Lung / Q000382:microbiology; D051379:Mice; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D010766:Phosphorylation; D011112:Polymyxin B / Q000494:pharmacology; D011485:Protein Binding; D015398:Signal Transduction; D013997:Time Factors; D014162:Transfection
chemical_list: D000900:Anti-Bacterial Agents; D004268:DNA-Binding Proteins; D004731:Endotoxins; D020672:I-kappa B Proteins; D018950:Lipopolysaccharide Receptors; D016328:NF-kappa B; C000606204:NFKBIA protein, human; C000606205:Nfkbia protein, mouse; D000072000:NF-KappaB Inhibitor alpha; D011112:Polymyxin B