Production of β -defensins by Human Airway Epithelia

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 95; no. 25; pp. 14961 - 14966
• Main Authors: Singh, Pradeep K., Jia, Hong Peng, Wiles, Kerry, Hesselberth, Jay, Liu, Lide, Conway, Barbara-Ann D., Greenberg, Everett P., Valore, Erika V., Welsh, Michael J., Ganz, Tomas, Tack, Brian F., McCray, Paul B.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences of the United States of America 08.12.1998; National Acad Sciences; National Academy of Sciences; The National Academy of Sciences
• Subjects: Antimicrobials; Bacteria; beta-Defensins; Biological Sciences; Bronchi; Cells, Cultured; Defensins; Epithelial Cells - metabolism; Humans; In Situ Hybridization; Infections; Inflammation; Interleukin-1 - pharmacology; Lung diseases; Lungs; Medical research; Messenger RNA; Peptides; Protein Biosynthesis; Respiratory diseases; Respiratory System - metabolism; RNA, Messenger - biosynthesis; Table salt; Washing
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.95.25.14961

Human β -defensins (HBDs) are antimicrobial peptides that may play a role in mucosal defense. Diminished activity of these peptides has been implicated in the pathogenesis of cystic fibrosis (CF) lung disease. We show that HBD-1 and HBD-2 mRNAs are expressed in excised surface and submucosal gland epithelia from non-CF and CF patients. The pro-inflammatory cytokine interleukin-1β stimulated the expression of HBD-2 but not HBD-1 mRNA and peptide in primary cultures of airway epithelia. HBD-1 was found in bronchoalveolar lavage (BAL) fluid from normal volunteers, CF patients, and patients with inflammatory lung diseases, whereas HBD-2 was detected in BAL fluid from patients with CF or inflammatory lung diseases, but not in normal volunteers. Both HBD-1 and HBD-2 were found in BAL fluid in concentrations of several ng/ml, and both recombinant peptides showed salt-sensitive bactericidal activity. These data suggest that in the lung HBD-2 expression is induced by inflammation, whereas HBD-1 may serve as a defense in the absence of inflammation.