Journal
JOURNAL OF IMMUNOLOGY
Volume 174, Issue 3, Pages 1608-1615Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.3.1608
Keywords
-
Categories
Funding
- NCRR NIH HHS [RR00059] Funding Source: Medline
- NHLBI NIH HHS [HL67992, HL07638, HL61234] Funding Source: Medline
- NICHD NIH HHS [2K12 HD27748] Funding Source: Medline
- NIDDK NIH HHS [P30DK54759] Funding Source: Medline
Ask authors/readers for more resources
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 beta-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 beta-defensin in human neonatal lung. HBD-2 mRNA expression was developmentally regulated, induced by the proinflammatory factor, IL-1beta, 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available