Secretion of complement components of the alternative pathway (C3 and factor B) by the human alveolar type II epithelial cell line A549

Citation
Yx. Zhao et al., Secretion of complement components of the alternative pathway (C3 and factor B) by the human alveolar type II epithelial cell line A549, INT J MOL M, 5(4), 2000, pp. 415-419
Citations number
26
Categorie Soggetti
Medical Research General Topics
Journal title
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
ISSN journal
11073756 → ACNP
Volume
5
Issue
4
Year of publication
2000
Pages
415 - 419
Database
ISI
SICI code
1107-3756(200004)5:4<415:SOCCOT>2.0.ZU;2-F
Abstract
The complement system participates in the local immune system of the lung. In this study, we investigated the secretion of complement components of th e alternative pathway (C3 and factor B) in the alveolar type II epithelial cell line A549. The levels of C3 and factor B protein in the culture medium were determined by enzyme-linked immunosorbent assay (ELISA). The C3 and f actor B mRNA expression was assessed by reverse transcription polymerase ch ain reaction (RT-PCR). The addition of interleukin (IL)-1 beta or tumor nec rosis factor (TNF)-alpha induced a dose- and time-dependent increase in C3 and factor B secretion. The addition of IL-6 or interferon (IFN)-gamma also induced a weak but significant increase in C3 and factor B secretion. Thes e responses at the protein level were also observed at the mRNA level. Furt hermore, the combination of IL-1 beta plus TNF-alpha induced a marked incre ase in C3 and factor B secretion. Similarly, IL-6 and IFN-gamma potently en hanced IL-1 beta or TNF-alpha-induced C3 and factor B secretion, respective ly. In this study, we demonstrated C3 and factor B secretion in A549 cells, and showed that the proinflammatory cytokines, IL-1 beta, IL-6, TNF-alpha and IFN-gamma, acted as potent inducers of C3 and factor B secretion. It is likely that alveolar type II epithelial cells are the local sites of compl ement biosynthesis, and that various cytokines act as regulators of this lo cal immune protection system.