Antibacterial activity of apical surface fluid from the human airway cell line Calu-3 - Pharmacologic alteration by corticosteroids and beta 2-agonists

Citation
Y. Zhang et al., Antibacterial activity of apical surface fluid from the human airway cell line Calu-3 - Pharmacologic alteration by corticosteroids and beta 2-agonists, AM J RESP C, 25(2), 2001, pp. 196-202
Citations number
35
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
ISSN journal
10441549 → ACNP
Volume
25
Issue
2
Year of publication
2001
Pages
196 - 202
Database
ISI
SICI code
1044-1549(200108)25:2<196:AAOASF>2.0.ZU;2-Z
Abstract
Calu-3 cells, a human lung carcinoma cell line with properties like serous cells of the upper airway, were used to develop an in vitro model for airwa y antibacterial activity. Calu-3 cell monolayers were cultured on permeable supports at an air-liquid interface. Apical surface fluid (ASF) was collec ted by washing; antibacterial activity was assayed by incubating ASF washin gs with bacteria for 18 h and counting surviving colony-forming units. ASF washings killed Escherichia coli and Pseudomonas aeruginosa. Antibacterial activity was salt sensitive and dependent on protein concentration. After w ashing, approximately 30 h were required before antibacterial activity reco vered to its initial level. After culturing with topical corticosteroids (b udesonide, triamcinolone, or beclomethasone, 0.1 mug/ml for 48 h), ASF anti bacterial activity was 4- to 10-fold greater than the ASF from control mono layers. The increase in antibacterial activity was dose-dependent. The beta (2)-agonists salbutamol and terbutaline (100 mug/ml for 48 h) decreased AS F antibacterial activity by 5- to 8-fold. The nonsteroidal anti-inflammator y agents ibuprofen and cromolyn sodium had no effect. Our results are most consistent with agonist-dependent changes in the composition of ASF antibac terial proteins. We conclude that Calu-3 cells synthesize and secrete antib acterial proteins and that clinical agents can alter these functions.