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a Department of
Pulmonary Medicine and Laboratory of Respiratory Cell Biology, Sapir
Medical Center, Meir General Hospital Kfar-Sava 44281 and Sackler
School of Medicine, Tel-Aviv University, Tel-Aviv, Israel, b Department of Otolaryngology
Correspondence to: Dr S Varsano email: Varsanos{at}green.co.il
Received 8 June 1999; Returned to authors 23 August 1999; Revised version received 7 January 2000; Accepted for publication 19 January 2000
BACKGROUND
The
interrelationship between human airway epithelium and complement
proteins may affect airway defence, airway function, and airway
epithelial integrity. A study was undertaken to determine (1) whether
unstimulated human bronchial epithelium generates complement proteins
and expresses cell membrane complement inhibitory proteins (CIP) and
(2) whether stimulation by proinflammatory cytokines affects the
generation of complement and expression of cell membrane CIP by these cells.
METHODSHuman
bronchial epithelium cell line BEAS-2B was cultured in a serum-free
medium. Cells were incubated with and without proinflammatory cytokines to assess unstimulated and stimulated generation of complement C3, C1q and C5 (by ELISA), and to examine the expression of
cell membrane CIP decay accelerating factor (DAF; CD55), membrane cofactor protein (MCP; CD46), and CD59 (protectin) by flow cytometry analysis.
RESULTSUnstimulated
human bronchial epithelial cell line BEAS-2B in serum-free medium
generates complement C3 (mean 32 ng/106 cells/72 h, range
18-52) but not C1q and C5, and expresses cell membrane DAF, MCP, and
CD59. Interleukin (IL)-1
(100 U/ml/72 h) and tumour necrosis
factor (TNF-; 1000 U/ml/72 h) increased generation of C3 up to a
mean of 78% and 138%, respectively, above C3 generation by
unstimulated cells. DAF was the only cell membrane CIP affected by
cytokine stimulation. Interferon (IFN)-
(10 U/ml/72 h) and TNF-
(1000 U/ml/72 h) increased DAF expression up to a mean of 116% and
45%, respectively, above that in unstimulated cells. MCP and CD59
expression was not consistently affected by IL-1, TNF-, or
IFN-.
CONCLUSIONSLocal
generation of complement C3 and expression of cell membrane CIP by
human bronchial epithelium and its modulation by proinflammatory
cytokines might be an additional regulatory mechanism of local airway
defence and may affect airway function and epithelial integrity in
health and disease.
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