Expression and activity of β-defensins and LL-37 in the developing human lung

Timothy D. Starner*, Birgitta Agerberth, Gudmundur H. Gudmundsson, Paul B. McCray

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

92 Citations (Scopus)


Immaturity of innate immunity contributes to the increased susceptibility of human neonates to infection. The lung is a major portal of entry for potential pathogens in the neonate, and human β-defensins (HBDs) and LL-37 participate in pulmonary innate immunity. We hypothesized that these antimicrobial factors would be developmentally regulated, expressed by neonatal pulmonary tissues, and participate in neonatal innate immunity. We found HBD-2 to be the predominant β-defensin in human neonatal lung. HBD-2 mRNA expression was developmentally regulated, induced by the proinflammatory factor IL-1β, and decreased by dexamethasone. Additionally, HBD-2 abundance in neonatal tracheal aspirates increased as a function of gestational age. HBD-1 had a lower level of expression compared with HBD-2 and was induced by dexamethasone. HBD-3 and LL-37 messages were not detected in airway epithelial cultures. Additionally, each antimicrobial peptide exhibited a unique spectrum of antimicrobial activity and salt sensitivity against bacteria commonly causing sepsis in the neonate. Lower levels of HBD-2 may be one factor contributing to the increased susceptibility of premature infants to pulmonary infections.

Original languageEnglish
Pages (from-to)1608-1615
Number of pages8
JournalJournal of Immunology
Issue number3
Publication statusPublished - 1 Feb 2005


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